High Potassium Foods

High potassium foods, low potassium foods and associated potassium symptoms info

 

Cellular Function And Potassium Sodium Ratio

What you eat determines how well all the cells in your body function. The potassium sodium ratio is the primary determinant of how well your cells function. This is because the potassium sodium ratio determines the electric field across your cell membranes. This electric field determines the shape and function of all the proteins in your cell. It does this by moving potassium and sodium around to change the electric fields in the cell.
38-PotassiumChannels

Cellular Electric Fields

Although the general concept has been known for quite a while, the details of these electric fields are only now being discovered. Computer simulations and experimental evidence are demonstrating how the electric field created by the potassium sodium ratio and the local electric fields in the proteins work.

Potassium and sodium are moved in and out of the cell by channels and pumps. X-ray crystallography has shown the atomic structure of some channels in their active state. The active state is when the channels are open, and sodium or potassium is moving through them.

However no such views of the atomic structure of channels in their resting state (when they are closed) have been done. And no views of the channels in intermediate states between the active and resting states are available. But multiple computer simulations have been done to show the missing positions of the channels, and to show how the channels function.

How Potassium And Sodium Control Cellular Electric Fields

The potassium and sodium balance in cells is maintained by channels and pumps. They move potassium and sodium from inside to outside and from outside to inside the cell. In doing so they change the electric field of the cell.

This change in the electric field changes the shape of the proteins that are in the field, much like the changing electric field in an electric motor changes the position of the rotor in the motor. Only, the channels and pumps are much faster than an electric motor.

The change in shape of the protein is how the protein functions. The functional result of the changed shape depends on the particular protein. In the case of voltage gated (VG channels) channels the changing shape of proteins results in an alternation of opening and closing the channel.

Voltage gated channels are protein channels through lipid membranes in the cell that let potassium and sodium (and a few other ions) move through them to go from one place to another. They open and close based only on changes in the electric field they sit in. Each type of channel is unique and lets only one type of ion through. Potassium channels let potassium through. Sodium channels let sodium through.

How A Poor Potassium Sodium Ratio Ruins Cellular Function

However if you do not eat enough potassium, or if you eat and retain too much sodium, you will have a less than optimal balance of potassium and sodium inside and outside your cells. This less than optimal balance will result in a less than optimal electric field to motor your cell processes.

If the electric field is stronger (or weaker) than it should be, then when there is a change in the electric field, the channel protein will have to move more (or less) to perform its function. This will result in taking a longer (or shorter) time to perform its function, and will result in incorrect timing of cell processes. This incorrect timing makes it more likely that the cell will function abnormally.

A Close Look At Channels

At present, x-ray crystallography studies of crystallized channels have shown the shape of some open (active) channels. However the shape of a closed channel has not been seen with x-ray crystallography. And none of the intermediate states between open and closed have been seen with x-ray crystallography.

But computer simulations of the resting state of the channel, and of the intermediate states of the channel, have been done. Multiple different methods have been used to create the simulations. And they have all given remarkably similar results. See http://jgp.rupress.org/content/140/6/587/suppl/DC1 for a beautiful video demonstration.

There was a similar situation in the 1980s when MRIs (also known as NMRs), which are also computed simulations, were done to show protein structures. Later x-ray crystallography studies confirmed these computer simulated models.

It is anticipated that when similar x-ray crystallography studies can be done on the channels, a similar confirmation will occur because there is a remarkable similarity in all of the present computer simulations. Thus there is a high probability that the simulations do correspond to what really goes on in the cell.

The Present Study

The present study (1) is a recent review of how these computer simulations were done, and a comparison of the simulations to show how similar their results are. Each simulation was done by a different group of researchers using different computer methods of molecular modeling, and different template x-ray structures. The results of these simulations showed very similar structures of the VSD (voltage sensing domain) of a potassium channel in its resting state.

Several findings have been confirmed by the similarities in the models. The models have shown that the VSD depends upon salt bridges for its shape. Movement of these salt bridges results in a screw-slide movement of the molecules, resulting in the opening and closing of the pore that lets potassium through. The image above shows the open and closed structures of a channel. More is written about salt bridges here and here.

These simulations also showed that VSDs must move through more resting states before activation when they start from a more negative membrane potential. This means that when the potassium sodium balance has changed, there is a change in how the VSDs function. If the electric field is stronger, the proteins in the gate must move more, and take longer to move, between open and closed. If the electric field is weaker, the proteins will have less movement before the pore will open or close.

Several aspects of the models have been confirmed experimentally. Portions of the VSD structure were later confirmed by experimental data. Distances that were predicted between certain atoms in the structure were also confirmed experimentally. The hope is eventually to see in experiments atom-by-atom movement in the structure over time. This would give experimental evidence to confirm the computer simulations.

The Importance Of The Potassium Sodium Ratio

Thus in addition to the interesting findings about how these channels open and close, the simulations also show the importance of the potassium sodium ratio. When the cellular potassium sodium ratio is not optimal, the electric field will not be optimal. And the movement of the protein in the channels will not be optimal, meaning potassium and sodium movement will not be optimal.

When the movement of potassium and sodium through the channels is not optimal, the timing of the all-important changes in electric field will be off. This leads to mistimed cellular processes and abnormal cellular function.

So we have evidence at the atomic level of how important the potassium sodium ratio is. Epidemiologic studies provided the first evidence. Later evidence came from animal and human group studies. Now at the molecular and atomic level, findings are consistent with the importance of the potassium sodium ratio.

If we do not supply too much sodium, and if we supply enough potassium to our body, our body will provide the correct amount to our cells. This will provide an optimal electric field for the very best function of our cells. However if too much sodium or not enough potassium is supplied, the electric fields in our cells will not be at an optimal level. This will result in less than optimal function of our cells, and less than optimal function of ourselves.

This poor cellular function shows up in assorted ways over various periods of time. The most common way it shows up is hypertension and its associated problems of stroke, heart disease, and kidney disease.
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1. An emerging consensus on voltage-dependent gating from computational modeling and molecular dynamics simulations. Vargas E, Yarov-Yarovoy V, Khalili-Araghi F, Catterall WA, Klein ML, Tarek M, Lindahl E, Schulten K, Perozo E, Bezanilla F, Roux B. J Gen Physiol. 2012 Dec;140(6):587-94. doi: 10.1085/jgp.201210873.

Salt Bridges And Potassium

Potassium in your food matters because your cells need enough of it to function properly. You need enough inside your cells to balance the sodium outside your cells. Your cells do their work by changes in the electrical field produced by moving potassium and sodium around. The changes in the electrical field change the shape of proteins in the cell. When the shapes of proteins change, your cells can extract energy from fuel (food), they can make cell structures, and they can unveil genes and translate genes.

In the last post we discussed how structural changes in the VSD of the gate that opens and closes potassium channels can affect how fast potassium can balance with sodium. Slight changes in the electric field of a cell can cause a difference in the shape of the VSD protein. This change in shape will allow potassium to flow through the channel or will stop it from flowing through.

Protein Molecules’ Shapes

Salt Bridge ChangeThe main determination of the shape of a protein is the sequence of amino acids in the protein. But there are multiple other factors determining the shape. Two major factors are the large cellular electrical field produced by sodium and potassium, and the smaller local electric fields within the protein.

The local electrical fields in a protein come from its amino acids. These fields are determined by the charges on the amino acids in the protein, by the distances between these local charges, and by any ions in the local field.

The force of the larger cellular electric field that the protein sits in is added to the local field forces. Thus this larger electric field influences the strength of local electric field forces, such as hydrogen bonds, salt bridges, electrostatic forces, and other local forces that give rise to the ultimate shape of the protein.

How A Protein Does Its Work

The last post discusses the importance of salt bridges in the function of the VSD. A change in position of six salt bridges in the VSD occurs when there is a change in the electric field across the membrane that the potassium channel sits in. This field change is created by movement of potassium and sodium across the membrane. This causes the protein’s shape to go back and forth, and perform its function of opening and closing gates on the potassium channel.

But you do not need to change multiple salt bridges to affect how a cell functions. A change in just one salt bridge is enough, as discussed in a recent study (1). Especially when the change results in a permanent structural change in a protein.

Severe Bodily Changes From A Salt Bridge Change

This recent study (1) of a salt bridge in an important nuclear protein showed a connection between the severity of a molecular change in the protein and the severity of what happens to a person’s body.

The structural protein (lamin A) that was affected is produced by the LMNA gene. Just like the VSD protein, it is also affected by the charge inside and outside the cell. This protein provides the structure of the nucleus of the cell, and plays a role in the function of the chromosomes. Its structure was changed when a single salt bridge in the protein was changed.

A salt bridge is a very small bond between 2 molecules that is not as strong as a covalent bond. It is composed of a hydrogen bond and an electrostatic bond combined. This post discussed how important salt bridges are in the potassium channels and pumps in cell membranes. Small changes in the electric field that the VSD of a potassium channel sits in changes its six salt bridges and its shape, so channel can do its work.

However a change in the local electric field of just one salt bridge can result in severe changes to a person’s entire body. This study showed that changing one salt bridge can result in massive skeletal abnormalities with an undergrowth of the jaw and collarbones. It can also result in thinning of the bones in the fingers, delayed closure of bony parts, overcrowding of teeth, thinning of the skin, growth retardation, and severe metabolic abnormalities such as lipodystrophy, insulin resistance, diabetes, and hypertriglyceridemia. All of this from a single amino acid change in a protein, resulting in a change in the strength of a salt bridge.

In this particular study, the researchers found 3 different types of changes in a single salt bridge of the protein lamin A. The researchers had 3 patients, each of whom had a change in a single amino acid at position 527 in the protein. This position normally has arginine. By predicting the strength of the salt bridge, they were able to predict how much of a change would occur in a patient’s tissues and organs.

Salt Bridge Changes

In the first case, leucine replaced arginine and led to loss of the salt bridge. Using computer modeling, the researchers predicted severe changes to the patient’s body because the protein structure was destabilized.

In the second patient, histidine replaced arginine, resulting in a weaker salt bridge, but not a loss of the salt bridge, as occurred in the first case. The researchers predicted that the structure of the protein would be destabilized, but less so than with leucine. This led to less severe bodily changes than occurred in the first case.

The third patient had a substitution of arginine with cysteine, which led to a disulfide bridge. This resulted in complete structural change of the protein and led to the most severe bodily change.

Thus with a computer modeling system from multiple bioinformatics sources, the researchers were able to predict the severity of the effect on a person from the severity of the effect on a protein. The effect on the protein came from the physical forces involved in a single salt bridge in a single structural protein. The researchers found that the more severe the change in physical forces between molecules, the more severe the effect on the patient.

Why The Study Is Important

This article shows the importance of the electric field that is created by the potassium and sodium concentrations inside and outside our cells. Small changes in this large electric field change the local fields in our cells’ proteins. These changes back and forth in local electric fields are how our cells do their normal work.

If the large electric field from potassium and sodium is too strong or too weak, the local electric fields may not be able to change adequately. If the local fields cannot change adequately, the protein cannot change shape enough to do its work. When this happens, the cell does not function well, and we do not function well.

Keep your cells functioning well by keeping a good balance of sodium and potassium inside and outside your cells. Eating meals with a high potassium sodium ratio is the best way you can provide your cells with what they need to function well.

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1. A novel homozygous p.Arg527Leu LMNA mutation in two unrelated Egyptian families causes overlapping mandibuloacral dysplasia and progeria syndrome. Al-Haggar M, Madej-Pilarczyk A, Kozlowski L, Bujnicki JM, Yahia S, Abdel-Hadi D, Shams A, Ahmad N, Hamed S, Puzianowska-Kuznicka M. Eur J Hum Genet. 2012 Nov;20(11):1134-40. doi: 10.1038/ejhg.2012.77. Epub 2012 May 2.

Potassium Channel Gates And Potassium Sodium Ratio

Why is the potassium sodium ratio so important in food? The reason is because it determines the size of the charge differential across cell membranes. And it is the charge differential across cell membranes that determine how well proteins in the membranes, and in the rest of the cell work. If there is too big of a differential, the proteins need a bigger change in charge to change shape and do work in the cell. If there is too little of a difference, the proteins may change shape too quickly or easily.

The last post discussed how changes in electric charges in the cell have optimal rates and an optimal voltage (optimal difference in charge across the membrane) to perform cell functions. So how do these charge changes occur? The charges change by moving ions across the cell membranes. A whole bunch of ions move from inside the cell to outside and others move from outside to inside.

Ion Channels

1r3jThe ions do this movement through channels, which are passive, and pumps, which are active and require energy. Some of the channels only need a change in the electrical field they sit in to open and close. Others need something, such as a protein or calcium, to attach to them in order to change in shape.

These channels that only need a change in charge have an area on them that senses when the electric field changes. This area is called a voltage sensing domain (VSD). The voltage changes when the electric charge inside or outside the cell changes.

The most common example is when a nerve fires. But almost all, if not all, of our cells perform their functions in a similar manner. When the electric charge changes in the cell, events in the cell occur that result in the cell performing its functions.

Each of these VSDs is similar in structure. They are present and retain the same basic structure from the most primitive organism to the most complex beings. When a cell structure is shared so extensively throughout living organisms, it performs an extremely important function. The electric field in the cell is the basis of all the functions in the cell.

Potassium And Sodium Make The Difference

Almost all of the difference in charge across the cell membrane is determined by the potassium and sodium inside and outside the cell. When this charge difference changes, potassium and sodium move. For a nerve cell depolarization, sodium moves inside the cell and potassium outside. When the nerve cell re-polarizes, sodium moves back outside the cell and potassium back inside.

The gate on a channel must open to allow the passage of potassium and sodium. And the gate must close to stop them from passing. The VSD on the channel initiates the opening and closing of the gate. Similar processes in muscle cells, heart cells, hormone cells and other functioning cells are initiated by the movement of potassium and sodium.

How Channels Open And Close

A recent article (1) discusses how these gates open and close. A very important part of how they open and close is based on the electric charge inside and outside the cell. This electric charge difference is known as a voltage potential across the membrane that these channels sit in. In addition to this voltage potential across the membrane there are smaller local electric fields determined in part by the voltage potential across the membrane, and in part by the amino acids in the protein which have charges with effects over shorter distances.

Changing the large electric field that results from this voltage potential affects all the protein molecules sitting in the field. One way the large electric field affects the protein molecule is by affecting the smaller local electric fields in the various parts of the protein. When the local fields change, the protein changes shape.

This article looked at the specific local fields in the VSD to determine how this VSD protein changed shape to open and close the channel gate. There is presently no way to directly measure the inter-atomic forces between the atoms in the gate. Instead, the researchers used a computer simulation based upon many known forces acting at the atomic level. The values of these known atomic forces are collected in multiple databases available to researchers.

The researchers found that the change in electric charge caused a change in the local electric field in salt bridges in the VSD. The change in the local electric field caused salt bridges in the protein in the VSD to rearrange. The rearrangement of the salt bridges caused the channel to close and the reverse resulted in them opening.

Salt Bridge

The salt in a salt bridge does not refer to table salt. It is called a salt bridge because the interaction between 2 ionized sites that sit close to each other in a protein is similar to the interaction between 2 ions of a salt. However the salt bridge has a hydrogen bond as well as an electrostatic interaction.

When the salt bridges rearrange, the protein changes shape, thus opening or closing the gate. This all happens in about 10 microseconds. If the local electric field is not quite right, the timing of the gate opening and closing is not quite right. In this particular study, the researchers found that the depolarization potential had to be complete before a repolarization could occur. If these channels do not function properly, the cell will not function properly.

The post last week showed that there is an optimal voltage and timing for proper function of the sodium potassium pump. The study discussed this week showed that there also is an optimal voltage and timing for proper function of these voltage dependent channels.

You might ask what all this molecular biology has to do with the food I should eat. If your goal is to eat food that will allow the cells in your body to function optimally, you will need to obtain food with enough potassium, and not too much sodium, so that the charge inside and outside your cells is at the proper level. If these charges are not at the proper level, the channels and the pumps inside your cells will work differently. And usually this means that your body will not function as well as it could.
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1. Microscopic origin of gating current fluctuations in a potassium channel voltage sensor. Freites JA, Schow EV, White SH, Tobias DJ. Biophys J. 2012 Jun 6;102(11):L44-6. doi: 10.1016/j.bpj.2012.04.021. Epub 2012 Jun 5.

Cellular Electric Field Effect

It is important to have high potassium foods as the basis of your diet. This is because the potassium sodium ratio of your food determines how well your cells function. Each of your cells needs a lot of potassium inside to balance the sodium outside the cell. This balance creates a difference in electric charge inside and outside the cell. This creates an electric field from the resulting electric potential (voltage) that affects every chemical process inside the cell. If the charge difference is less than optimal, everything the cell does is less than optimal.

An enormous body of scientific work has been done over the years on the details of how this electric field affects your cells. Researchers have done work showing how the field affects the shape of proteins in your cells, and how it affects the speed of chemical processes in your cells.

Electrical potential and field lines between two wires
Cellular Electric Field Effects

The cellular electric field affects the shape of the proteins that send signals. It affects the shape of the proteins that transport ions and molecules. It affects the shape of proteins in the channels that move ions through membranes, and thus affects the movement of those ions. And similarly it affects the pumps that actively move ions and other molecules against their concentration gradient. The ion movement triggers many of the cellular functions.

One very important effect of this cellular electric field is its effect on a critical cellular pump. This particular pump keeps the potassium and sodium balanced inside and outside your cells. It has had various names. Presently the most popular is Na+/K+-ATPase (sodium-potassium adenosine triphosphatase, also known as Na+/K+ pump, sodium-potassium pump, or sodium pump.) The balance of sodium and potassium is so important that estimates have been made that as much as 70% of all your resting energy is spent on maintaining this balance. 20% of your total energy, and up to 70% of the energy used by some cells is spent on this specific pump.

Because this pump is so important, a great deal of research has been devoted to studying it. And because the electric field in the cell has such a major influence on how well the pump works, a great number of studies have been done on the effect of the field on the pump. An early study from 1994 showed how rapidly fluctuating fields affect the sodium potassium pump.

The Study

In this study (1) the researchers isolated the sodium-potassium pumps in cell membranes. They then applied randomly fluctuating electric fields to the pumps. Then they observed the movement of ions across cell membranes. By applying the fields in varying strengths and by varying the frequency that the electric fields changed at, they were able to find the optimal voltage (strength of the field) and the optimal rate of change of the field for maximal movement of the ions.

What this study showed is that there is an optimal rate at which the pumps in the cell membranes can operate. It also showed that this optimal rate is controlled by the voltage across the membrane and by how quickly this voltage changes.

How Cellular Voltage Changes

This optimal voltage is controlled by the ion balance. Ions are charged atoms or polyatoms such as potassium, sodium, calcium, chloride or bicarbonate. The greatest contribution to the voltage is the balance of potassium and sodium inside and outside your cells. Potassium sodium balance is obtained only when you get adequate amounts of potassium and limited amounts of sodium in your diet.

The speed of the voltage change varies for different types of cells. The voltage change results from a change in the electric charge inside and outside the cell. These changes in charge occur when potassium and sodium move back and forth across the cell membrane in channels or pumps. This movement occurs very rapidly – in microseconds. For some channels working properly, over a million ions per second can move through the channel.

What Voltage Changes Do In Cells

This results in cellular proteins changing shape rapidly. When the shape-changing proteins are located in channels and pumps that cross membranes of the cell, ions such as sodium and potassium move through them or are stopped from moving through them, depending on the resulting shape of the proteins. The shape changes occur very rapidly. And thus the voltage changes occur rapidly.

The effect on other proteins in the cell is to change their shapes also. These rapid protein shape changes allow cells to do what they are supposed to do. And when your cells do what they are supposed to do, you can do all the things that you want to do (well, maybe not all the things.)

Now this rapid movement does not mean that faster ion movement is always better for you. But it does mean there is an optimal movement that is determined by the electric field in the cell. And the electric field is determined by the potassium sodium ratio.

A Case Of A Slowed Pump Leading To Longer Life

In certain cells, slowing down some of the cell processes can result in the body functioning better. We saw this in a study that was done on the sodium potassium pump in kidney cells, discussed in this post. When the pump was slowed in these kidney cells, there was less sodium reabsorption. And when less sodium was reabsorbed, there was less excess sodium and less storage of sodium in the body. This resulted in lower blood pressure. And in Sardinians this slower reabsorption of sodium in the kidney resulted in lower blood pressure and longer life, as discussed in this post.

Presently researchers are investigating how the local charges inside the proteins (including the proteins in the pumps and channels) are affected by the overall electric field the protein lies in. And in turn how the change in local charges affects the shape of the protein, how the protein functions and how improper function causes deformities and disease in people. For any given genetic make-up, the electric field is affected by the potassium sodium ratio.
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1. Recognition and processing of randomly fluctuating electric signals by Na,K-ATPase. Xie TD, Marszalek P, Chen YD, Tsong TY. Biophys J. 1994 Sep;67(3):1247-51.

Longevity Gene GWAS

Life span has increased greatly in the last 200 years. But many of the extra years are not lived while in good health. It is been estimated that in modern society only 75 to 80% of life is spent in good health. But there are populations in which older people remain in good health throughout old age. There have been various types of studies to find out whether there is a genetic component to longevity, that is, a longevity gene. Estimates are that approximately 25% of life span variation is due to genetics.

Human genomeA Recent Longevity Gene Study

Despite all this interest, until a recent study there had been only one longevity gene candidate that was found associated with longevity. The present study (1) did a meta-analysis of Genetic-Wide Association Studies (GWAS) for longevity in the older European population. This study found one additional longevity gene (gene associated with longevity).

The researchers felt that this additional longevity gene works by reducing the risk of dying from stroke. They also found it to be associated with lower blood pressure in middle-aged Europeans. These two associations make it very likely that this longevity gene is associated with either sodium or potassium control in the cell. However, the researchers did no studies on the function of the gene.

The longevity gene that this study discovered was not the same gene as the gene that was discussed in the post about the Sardinian centenarians. The report about the Sardinian gene was published in January of this year, and was discovered by a targeted genetic study, not by a GWAS. That report showed that a high percentage of older Sardinians had a gene variant that slowed sodium reabsorption in the kidney.

Too Many Variables

Because the present study involved the general European population, there was a greater mixture of genes and environmental factors than in the Sardinians. This greater mixture makes it very difficult to find genes that contribute to longevity. If there are multiple biochemical pathways with potential longevity genes that are affected by environmental factors, there will be too many variables to account for.

Each potential longevity gene interacts with environmental factors to determine longevity. Because there are so many variants of each of these genes, it would be expected that any particular variant associated with longevity would be rare. This means that none would stand out in a GWAS. More targeted genetic studies in more uniform populations, such as was done in the Sardinian study, are more likely to find genes associated with longevity.

Sardinian Study

In the Sardinian study the Sardinians were relatively uniform in their genetics, having little contribution from genes outside of Sardinia. This genetic isolation has been for several centuries, if not longer. So there has been less chance for a mixture of genes and their variants. The genes that would contribute to longevity would not be as varied, and it would be easier to find contributing variants.

Also the Sardinian study was done in families living as herders in a mountainous area, providing a greater environmental uniformity. Since their physical activity and diet were more uniform than in the general European population, these well known environmental factors would have less influence on differences in longevity.

Approaches other than a Genome-Wide Association Study (GWAS) are needed to find genes associated with longevity. A GWAS involves screening many thousands of genes. A more focused study on some of the areas where there are a great number of centenarians or older individuals, and where there has been little genetic mixture and environmental variation will be more likely to find other genes associated with healthy longevity.

Other Approaches

Because of the high prevalence of hypertension, cardiovascular disease and strokes in old age, and the reduction in function they cause, the genes associated with these diseases would be the best early choices to target in studies looking for longevity genes. As discussed here, many of the genes involved in hypertension are variants involving potassium channels, sodium channels, and calcium channels. In addition to these genes, gene variants in sodium and potassium transporter proteins, and sodium potassium ATPase pump proteins would be good genes to examine.

One of the Blue Zones, made popular by Dan Buettner, would be a good place to start targeted longevity gene studies. Sardinia was one of the Blue Zone areas, and it made possible discovery of a sodium reabsorption gene that may have contributed to the longevity of Sardinians. And some of the other Blue Zones, as well as Sardinia, may provide good populations in which to study these genes.
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1. Genome-wide association meta-analysis of human longevity identifies a novel locus conferring survival beyond 90 years of age. Deelen J, Beekman M, Uh HW, Broer L, Ayers KL, Tan Q, Kamatani Y, et al. Hum Mol Genet. 2014 Aug 15;23(16):4420-32. doi: 10.1093/hmg/ddu139. Epub 2014 Mar 31.

Salt Sensitivity Test And Hypertension

High potassium foods can help prevent hypertension. With a high potassium to sodium ratio in the diet a great deal of hypertension and the problems associated with hypertension can be prevented. One way to categorize hypertension is to divide it into salt sensitive and salt insensitive hypertension. People with salt sensitive hypertension have a larger elevation of their blood pressure than salt insensitive people when they take in salt. Even when their blood pressure is normal, the salt sensitive people will have increased mortality. And they will have an increase in the problems that are associated with hypertension, such as heart attacks and strokes. It has been estimated that 26% of people with normal blood pressure have salt sensitivity.

Test tubeA Simple Salt Sensitivity Test

It would be helpful to be able to determine who has salt sensitivity so that salt sensitive individuals could have strong advice concerning their salt intake. At the present time, there are a few tests that doctors can run to determine salt sensitivity. However they involve testing that is more complicated than taking a simple blood sample or a simple urine sample. Some researchers recently found a much simpler way to determine salt sensitivity (1). And in doing so, they found a linear relationship between a gene change and salt sensitivity.

The researchers found two different genes in kidney cells that they could test in cells that are shed into urine. These two genes are known to be responsible for a large percentage of sodium reabsorption by the kidney. The genes specifically make proteins that transport sodium in the kidney cell.

First the researchers tested subjects using the usual tests for salt sensitivity. Between one and five years later they checked for the two genes in kidney cells in the urine of these same subjects. They found a linear correlation between changes in these genes and salt sensitivity.

How The Test Helps

This provides a simple test that would allow doctors to advise their patients about salt intake. The standard tests used now are more complicated and involved, and only used for someone with hypertension. They would be hard to justify using for someone with normal blood pressure. And the test may provide the confirmation needed to motivate those salt sensitive patients who otherwise would not reduce their salt intake.

Almost everyone who is healthy would benefit from a high potassium sodium ratio in their diet. But there is some debate about whether increasing potassium, or lowering sodium, or simply improving the ratio is more important. A helpful study these researchers could do would be to study the potassium sodium ratio of the diet along with gene changes in test subjects. It could possibly help resolve the debate by correlating the potassium sodium ratio with blood pressure changes and gene changes.

This type of study would be especially helpful for those patients with so much kidney, heart, and blood pressure problems that they actually may be put at greater risk when put on a very low sodium diet. It may be that these patients would be helped more by increasing their potassium intake, while keeping their sodium intake at a higher level than necessary for healthy people.
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1. A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: the virtual renal biopsy. Gildea JJ, Lahiff DT, Van Sciver RE, Weiss RS, Shah N, McGrath HE, Schoeffel CD, Jose PA, Carey RM, Felder RA. Clin Chim Acta. 2013 Jun 5;421:236-42. doi: 10.1016/j.cca.2013.02.021. Epub 2013 Feb 27.

A Potassium Channel Hypertension

Hypertension affects over 1 billion people. It contributes to 7 million deaths each year. Inheritance is felt to affect about 30 to 35% of blood pressure levels. The other 65 to 70% is under our control. The controllable aspect is influenced by physical activity, habits and the food we eat. There are two main components of our food that influence blood pressure levels. Sodium is one component. And potassium is the other. The ratio of these two components inside and outside our cells is what determines blood pressure. What we eat is what determines how much of each component is available.

Potassium Channel ProteinGenetics And Potassium

And genetics is what determines how the available potassium and sodium components are used. The interaction of these components with genetics is what determines the electrical charges within the cell.

You might say “What do I care about the genetics of blood pressure?” The reason you should care is because genetics is what determines how strong a potassium sodium ratio in your diet is needed to generate the proper electrical charges to prevent hypertension and to promote good health. Someone else with different genetics may lower their blood pressure with a diet that has no effect on your blood pressure.

The last post discussed genetic changes affecting how sodium is moved around in the cells (transporter proteins). Another previous post discussed an instance of genetic changes that influenced potassium’s effect on the manufacture of aldosterone (one hormone that raises blood pressure). There’s been a recent study (1) of changes in a potassium channel in our cells that affects aldosterone secretion.

This Study

In this recent study the researchers discovered a change in a potassium channel that is a major cause of secondary hypertension. Remember that normally an increase in aldosterone leads to an increase in sodium reabsorption in the kidney and a rise in blood pressure. Normally when there is an increase in potassium outside the cell, potassium will move into the cell.

In certain adrenal gland cells the resulting increase in membrane polarization (the difference in electrical charges across the membrane) leads to less aldosterone secretion. The lowering of aldosterone leads to less sodium reabsorption in the kidney and thus lower blood pressure. In some people blood pressure is high and does not come down, because they have a gene that prevents this normal sequence.

In this particular study, a gene variant was found that affected part of a potassium channel. The change meant that the channel no longer allowed only potassium to pass. The channel allowed sodium to pass through the potassium channel as well as potassium. This led to a decrease in the membrane polarization and an increase in aldosterone secretion. This increase in aldosterone meant that blood pressure increased.

The researchers found two variants, each of which let more sodium in. One variant was not as severe and let less sodium into the cell than the other variant did. This less severe variant led to an increased number of adrenal cells, resulting in overgrowth of the cells. However the more severe variant let in so much sodium that the cells died.

The change in blood pressure was not as bad in people with the more severe variant. The more severe variant resulted in fewer cells left alive to overproduce aldosterone. The less severe variant resulted in more and more cells, so there was more and more aldosterone.

To eliminate other possible explanations for the cell death, the researchers then grew the cells with the more severe variant in culture and did an experiment with the cells. The experiment showed that the cell death was indeed because of too much sodium getting inside the cells.

Although the involved cells died, the individuals with these cells did not die. The researchers felt that nearby immature adrenal cells replenished the dead cells. As the cells matured, they would overproduce aldosterone for a while and then they too would die. Some cells that overfunctioned may have stayed alive because other mechanisms in the cell compensated for the excess sodium inside the cell. Other studies indicated that this could occur if there were an increase in the sodium potassium pump removing sodium, or if there were a change in the activity of other potassium channels.

Two Concepts

So there are two important concepts that this particular study supports. It supports the importance of the balance of sodium and potassium inside the cell for proper function. And it supports that the variability in blood pressure is related to the function of the potassium channels, as well as the sodium channels and the sodium potassium pump.

The critical variable in each of these cases is the electrical charges across the membranes in the cell. These charges are determined by the potassium and sodium balance in the cell. The potassium and sodium in the cell are determined by the activities of the channels and pumps, and the proteins that transport potassium and sodium. When the membrane electrical charges change in the kidney, sodium reabsorption is affected, as discussed in the previous post. When the charge changes in the adrenal cells, aldosterone secretion is affected, as discussed in this present post.

When Genetics Meets Diet

Each of us have genes that vary from the genes in other people. Some of these gene variations help some of us to have better protection against hypertension than others have. But it is important for all of us to maintain an optimal potassium sodium ratio.

We can do nothing to change the differences in our genetic makeup. However if we do not have extreme genetic changes, such as the syndromes discussed in some recent posts, we can control how well our cells function. We can better control how well our cells function by controlling the potassium sodium ratio in our diet. Some of us will find good control with a ratio of 2 and some will need a ratio over 5. However, a satisfactory ratio can be found for the vast majority of us.
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1. Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Scholl UI, Nelson-Williams C, Yue P, Grekin R, Wyatt RJ, Dillon MJ, Couch R, Hammer LK, Harley FL, Farhi A, Wang WH, Lifton RP. Proc Natl Acad Sci U S A. 2012 Feb 14;109(7):2533-8. doi: 10.1073/pnas.1121407109. Epub 2012 Jan 30.

Salt Handling And Hypertension

There have been a large number of studies of genes associated with hypertension. It is been estimated that heritability contributes to about 30-35% of blood pressure levels. A high dietary sodium and low potassium intake interact with certain genes to determine blood pressure. Genome-Wide Association Studies (GWAS) have found a great number of genes associated with hypertension. Most of these genes involve sodium or potassium in one fashion or another. Many of the genes determine either channels that sodium or potassium pass through, transporter proteins for the ions, or ion pumps. A recent review (1) of several salt handling (sodium handling) genes in the kidney was done in 2014.

Salt Handling Gene ChartKidney Salt Handling

Each gene for salt handling in the cells of the kidney has rare variants. Although any individual gene variant is rare, there are a fair number of them in total. There are so many that these rare variants are probably what account for the wide variation in blood pressure, and the wide variation in blood pressure’s sensitivity to salt (2).

There are two well known inherited syndromes, known as Gitelman’s and Bartter’s syndromes, which have been proven to be caused by such variants. These salt handling genes affect sodium reabsorption and cause salt wasting by the kidneys.

And they show how there can be a variation in how such genes affect people. Bartter’s syndrome causes serious health problems very early. It often presents while the child is still in the womb, and almost always before age 6. Gitelman’s causes similar problems, but varies by being less severe. It usually does not present until adolescence or early adulthood. In some people it is so mild that it may go undetected.

Other Salt Handling Variants

There are only a few genes involved in these two syndromes. However there are many other gene variants that affect sodium movement in the cell, and sodium reabsorption in the kidney. And many more that affect potassium in the cell. These variants have more subtle effects, and would be expected to take longer to have a noticeable effect on health.

Since each individual gene variant is rare, only about 1% of the population is estimated to be a carrier of any particular variant. However because there are estimated to be a great number of variants, they are felt to commonly contribute to blood pressure variation. But the result would not be as extreme as occurs in these two known salt wasting syndromes.

Only a few of the gene variants associated with hypertension are felt to cause an increase in gene function. We discussed here one of the variants that increased the function of a potassium channel in certain adrenal gland cells. The original study (3) finding this increase in function stimulated a great deal of research.

The subsequent research resulted in an estimate that 90% of gene variants in channels reduce the function of the channel. This reduction in function is known to result in a reduction in the electrical charge within the involved cells.

Among effects of a reduced charge is slower passage of ions. In the case of kidney cells, the major salt handling variant is involved in the reabsorption of sodium. This slower passage of ions means less reabsorption of sodium by the kidney.

Effect Of Less Salt Reabsorption

When less sodium is reabsorbed a person is protected against a high intake of sodium. These people can eat more sodium and still not have a rise in blood pressure. And this protection against hypertension lasts throughout the person’s lifetime.

This particular study (1) reviewed 3 genes involved in the sodium reabsorption in the kidney. Each of these 3 genes had a large effect on blood pressure. Depending upon the exact type of effect there will be a variation in the amount of sodium resorbed, and thus in the susceptibility to high blood pressure. The chart shown above is adapted from (2). It shows the mean systolic blood pressure for those who do not carry one of the variants, and the lower systolic pressure for those who do carry one of the variants.

We discussed a similar gene in the post here about the Sardinian centenarians. Although through a slightly different mechanism, the result of the gene variation was less sodium reabsorption. This particular gene was present in 14% of the centenarians, which is much higher than the non-variant gene in the general population. In fact it is approximately 14 times as common as the 1% variation estimated for genes of this sort.

Because of this high multiple, it is likely that this gene contributes to the longer functional life found in the Sardinian centenarians. As will be discussed in a future post, the activity of these types of genes is more of a factor contributing to a longer life than is the effect from the pressure itself. The electrical charges within the cell are what matters. The electrical charges determine how your cells function, and thus how well your body functions.

Why Some People Have Less Effect From Salt

Thus we can see that the variability in blood pressure is related to the gene variants in the potassium channels, sodium channels, potassium transporters, and sodium transporters, as well as the sodium potassium pump. The interaction of these cellular structures determines the electrical charges within the cell. If the cells with gene variants are located in the heart, the result is a greater or lesser susceptibility to heart failure, as discussed in this post. If they are in the adrenal gland, they will affect blood pressure as discussed in this post. If they are in the kidney, they will affect sodium reabsorption and thus also affect blood pressure. And if they are located in all cells throughout the body, the results will be determined by the degree to which each cell’s function is affected.

If the estimate of 30-35% of blood pressure being genetic is broadly applicable to other functions of the body, then 65-70% of how well your body functions is not genetic. The choices you make in diet, physical activity, and habits (smoking, for example) are more important than genetics.

Too Early For Gene Profiles To Help You

Genetic studies are all in an early stage of application to human health. Although they are consistent with the importance of the potassium sodium ratio in the diet, they need further studies (the usual caveat of the scientist) to show the specifics of the genetic interaction with the dietary potassium sodium ratio. It is doubtful that there will ever be a population study that will show specifically that the potassium sodium ratio has a linear relationship with mortality for hypertension.

Higher Potassium Sodium Ratio Helps

However multiple epidemiology studies have shown the importance of potassium and the importance of sodium in determining blood pressure. There have also been multiple animal studies showing how different levels of potassium and sodium in the diet affect cells in the animals. These types of genetic studies show the variations in cells that can account for the effects in the animals. If more studies are done with pure genetic variants in animals, then the diet can be varied in the genetically variant animals to show a relationship of diet to cellular changes, such as was done in the series of heart failure studies discussed here.

Such studies will make it possible to know how high a potassium sodium ratio you need in your diet to avoid the problems of hypertension. Specific gene combinations can be assessed for the ratio that prevents the electrical charge changes leading to cellular dysfunction. You will be able to adjust your diet to your genetic profile.

It will be unusual that anyone will need more sodium than the present minimal recommendation from the Institute of Medicine. Salt wasting conditions, such as Gitelman’s and Bartter’s syndromes, would be such a situation, but are quite rare. And they are usually discovered at an early age. Other conditions requiring more sodium are unusual in the absence of disease.

Most people will need a higher potassium sodium ratio in their diet than they get in the typical American diet. But the ratio to protect against the health problems associated with hypertension will vary. Some will only need a slightly higher ratio, and others will need more. But the vast majority will be able to find a ratio in their diet that will protect against hypertension and its potentially devastating effects.
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1. Rare mutations in renal sodium and potassium transporter genes exhibit impaired transport function. Welling PA. Curr Opin Nephrol Hypertens. 2014 Jan;23(1):1-8. doi: 10.1097/01.mnh.0000437204.84826.99.

2. Rare independent mutations in renal salt handling genes contribute to blood pressure variation. Ji W, Foo JN, O’Roak BJ, Zhao H, Larson MG, Simon DB, Newton-Cheh C, State MW, Levy D, Lifton RP. Nat Genet. 2008 May;40(5):592-9. doi: 10.1038/ng.118. Epub 2008 Apr 6.

3. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Choi M1, Scholl UI, Yue P, Björklund P, Zhao B, Nelson-Williams C, Ji W, Cho Y, Patel A, Men CJ, Lolis E, Wisgerhof MV, Geller DS, Mane S, Hellman P, Westin G, Åkerström G, Wang W, Carling T, Lifton RP. Science. 2011 Feb 11;331(6018):768-72. doi: 10.1126/science.1198785.

Sodium Reabsorption Gene & Hypertension

Sardinia has a Blue Zone, made famous by Dan Buettner for its high percentage of centenarians. Due to its long-standing isolation, low immigration rate, and fairly uniform lifestyle, Sardinia is a great location to study genetic traits associated with longevity. There have been multiple studies of older Sardinians, including studies of the genetics of hypertension. Many genes affect hypertension. As discussed here, a Genome-Wide Association Study (GWAS) is a screening method to look for possible genes associated with a disease. It is especially helpful for diseases involving multiple genes, such as hypertension. However, it only shows an association. After screening, other methods are needed to determine if and how a gene affects a disease. A recent article (1) used some of these other methods to show that a particular sodium reabsorption gene (ATP1A1) that was not found by GWAS was involved in hypertension in older men in Sardinia.

Sodium reabsorption gene productSodium Reabsorption Gene

Primary hypertension is divided into 2 large categories – salt sensitive and non-salt-sensitive. In salt sensitive hypertension small increases in sodium in the body lead more easily to hypertension. The kidneys play a large role in hypertension because they reabsorb sodium. The reabsorption may lead to more sodium in the body.

In this recent study, researchers showed a major influence on blood pressure from a change in a gene (ATP1A1) that is involved in regulating the reabsorption of sodium by certain cells in the kidney. This sodium reabsorption gene is also involved in maintaining the sodium potassium balance in the cells that line blood vessels. When there is imbalance, the vessel lining cells become stiffer.

This particular gene is a gene that regulates the sodium potassium ATPase pump. The sodium potassium ATPase pump comes in several variations, but there is only one variation found in these particular kidney cells and in the blood vessel lining cells. Thus when this gene is affected, it has a major effect on how much sodium is reabsorbed by the kidneys and how stiff the blood vessels are. If the effect is to slow down the pump, less sodium is reabsorbed in the kidney, and the effect on blood pressure of excessive sodium in the diet will be less.

The Study

The researchers studied several hundred of the older men and women in Sardinia for two forms of this gene. They looked at 678 older (> 60 years old) Sardinians and determined the difference in blood pressure in those with the common form of the gene and those with a variant of the gene. In women the difference in the sodium reabsorption gene produced no difference in blood pressure. But in the men there was a large difference in blood pressure.

After finding that those men who had the variant had lower blood pressure (12mm Hg systolic and 6 mm Hg diastolic) than those with the usual gene, the researchers checked that the common gene and its variant both were functional. They used the two variations in cell lines grown in tissue culture and found that both gene variations were functional.

Then they raised mice with the altered gene and found a difference in blood pressure compared to those mice with the unaltered gene. Those with the altered gene produced 58% less protein from the gene and had much lower blood pressure (17 mm Hg lower systolic).

Although this gene is not the only cause of high blood pressure, this study shows that a change in this sodium reabsorption gene will cause a change in blood pressure in humans as well as mice. This is the kind of confirmational experiment that is needed when association studies are done on human populations.

Not Just Another Association Study

By testing a hypothesis with experiments, fewer misinterpretations of association studies will occur. In this case, the researchers saw an association of different blood pressure levels with two variations in a gene in humans. They tested the hypothesis that the two variations of the gene affected blood pressure differently. First they isolated the different variations of the gene and showed that both variations were functional. Then they showed that the uncommon variation slowed sodium reabsorption by certain kidney cells. Finally they showed that the two different variations of the gene had the same effect on blood pressure in mice as in humans.

So we have another piece of evidence showing the importance of the potassium sodium ratio in hypertension. The model proposed by Dr Guyton, discussed here, and now in medical textbooks has another piece supporting it.

In this particular case, the study shows the importance of the sodium potassium pump in the kidney to maintain a proper level of sodium and to prevent too much sodium from accumulating in the body. This study provides another piece of evidence that the accumulation of sodium in the body leads to hypertension, and that the potassium sodium ratio is important for blood pressure.

Food Tables

Links to food tables can be found by using the List Of Posts tab at the top of the page.
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1. A Functional 12T-Insertion Polymorphism in the ATP1A1 Promoter Confers Decreased Susceptibility to Hypertension in a Male Sardinian Population. Herrera VL, Pasion KA, Moran AM, Zaninello R, Ortu MF, Fresu G, Piras DA, Argiolas G, Troffa C, Glorioso V, Masala W, Glorioso N, Ruiz-Opazo N. PLoS One. 2015 Jan 23;10(1):e0116724. doi: 10.1371/journal.pone.0116724. eCollection 2015.

Aldosterone Secretion, Genes And Diet

A high potassium diet is the single most important factor to prevent hypertension. There is more extensive evidence for the role of the dietary potassium sodium ratio than for any of the other factors that may be involved in hypertension. There is evidence from epidemiological studies, population studies, basic physiological studies, and animal and tissue studies. Presently many studies are being done at the cellular and molecular levels to determine how processes at these levels cause hypertension.

We previously discussed, in this post, how a fully developed hypertensive heart failure model has shown the importance of a high potassium diet. The model is complete from the level of the heart organ to the level of molecules in the heart cells.

Aldosterone SynthaseAldosterone Secretion, Potassium And Hypertension

The model for aldosterone secretion by the adrenal gland is not as complete as the heart failure model. This is an important model because of the central role of aldosterone and the RAAS (renin-angiotensin-aldosterone system) in the development of hypertension. Potassium and the potassium sodium ratio play a central role here, just as they do in hypertensive heart failure.

By studying at the cellular level abnormal secretion of aldosterone by adrenal gland cells, such as occurs in primary aldosteronism, researchers can more fully understand how hypertension occurs. And they can possibly devise methods for how it can be prevented.

Primary aldosteronism is the main cause of secondary hypertension. Sometimes it runs in families. Sometimes it is caused by a tumor in the adrenal gland. It signifies that too much aldosterone is being produced by the adrenal gland(s) without outside stimulation. This is one of the same mechanisms that cause primary hypertension. And the end result is the same – high blood pressure.

Hypertension Genetics

By studying the cellular abnormalities in primary aldosteronism researchers can also learn a great deal about how primary hypertension occurs. In 2013 a European Journal of Endocrinology published its prize lecture (1) about the genetics of primary aldosteronism. The publication gave a nice summary of what was then known about primary aldosteronism at the cellular and genetic level. The publication reveals a great deal about how potassium can affect adrenal cells. The article also reveals at the cellular level how an increase or decrease in the blood level of potassium causes changes in aldosterone secretion, and thus in blood pressure.

The report discusses the multiple studies done on adrenal cells, many of which the author’s group did, especially in primary aldosteronism. The author discusses genetic studies on animals and human genomes. These studies have identified genes that are associated with increased aldosterone. Many of the abnormal genes were found to control the proteins in potassium channels, and the proteins involved in transporting potassium for the sodium potassium ATPase pump.

These abnormal proteins cause these channels and pumps to handle potassium so poorly that there is not enough potassium inside the cell to maintain the electrical charges needed for normal cell function. This is the same problem that occurs when not enough potassium (or too much sodium) is in the diet. The result is excessive secretion of aldosterone and a rise in blood pressure.

The Basics

Before discussing the article, let’s review the previously known basics. Many years ago researchers showed that an increase in extracellular potassium leads to an increase in aldosterone secretion into the blood stream. This initiates a series of reactions that lead to an increase in blood pressure. However the increase in blood pressure is just one of many effects previously discovered. An excessive aldosterone blood level, even without an increase in blood pressure, damages the cardiovascular system and the kidney.

Today’s Research

Much research today focuses on what happens inside cells. To study aldosterone secretion, molecular pathways inside the cell and the genes that affect the pathways are being studied. Much of the work is being done on mice with experimentally produced changes in their genes. They have what are called knockout genes, which are specific genes that no longer function.

Many of the genes leading to excessive aldosterone secretion are genes that affect the electrical charge of the cell membranes in the cells that secrete aldosterone. The electrical charge is determined by the function of potassium channels, sodium potassium pumps, and intracellular calcium. Calcium controls much of the signaling inside the cell, and is affected by channels and pumps itself.

One of the genes that was studied was the gene that makes the enzyme (pictured above) that makes aldosterone in the adrenal cells. Potassium outside the cell (and angiotensin II) regulates the gene that makes this enzyme. Very minor changes in the extracellular potassium concentration control a signaling cascade. The potassium causes a change in the calcium concentration inside the cell. The calcium change starts a cascade of signaling molecules. The final signaling molecule reaches the DNA in the nucleus to upregulate (or downregulate) the gene so more (or less) enzyme is made.

This cascade happens within minutes of the change in potassium concentration. And it continues to occur for days (even years) when there is chronic stimulation. There are a great many specific types of potassium channels in the cells that make aldosterone. Changes in any of these specific channels affect the electrical charge of membranes in the cell. This in turn affects molecular reactions in the cell. These reactions affect the production and secretion of aldosterone. An increase in aldosterone secretion occurs with these abnormal genes, even when renin (another molecule affecting blood pressure) stays low.

Circadian Rhythm And Hypertension

Interestingly, the researchers also discovered how our circadian rhythm was involved in aldosterone secretion. One of the genes that was knocked out in these mice was a gene that is a core gene for the circadian clock. This circadian clock gene was found to affect aldosterone secretion from the adrenal gland cells. The researchers found that high salt intake increased the secretion of aldosterone in these animals. Furthermore they found that a constant daily salt intake resulted in aldosterone-dependent weekly rhythms of sodium storage (along with water weight) in the body.

Genome Wide Association Studies (GWAS)

This method has been used to identify genes involved in many different diseases. For diseases related to aldosterone, DNA arrays from patients with adrenal tumors and familial adrenal syndromes are used to study a large quantity of genes. Variations in how frequently a gene occurs show an association that can be further investigated as possibly causing a change in aldosterone secretion.

These studies are the type of studies we discussed here. That post discussed a study that identified 130 hypertensive genes. The majority of the genes were associated with potassium, sodium and calcium activity.

Other Genetic Methods

The author’s group has used other genetic methods to identify genes that lead to excessive aldosterone secretion. These genes involve some specific potassium channels that allow calcium in the interior of the cell to start the cell signaling process for aldosterone secretion.

Another pair of genes they identified affects proteins carrying potassium to the sodium-potassium-ATPase pump. They found that the pump was slowed, resulting in a change in the electrical charge of cell membranes that led to more aldosterone secretion.

There have been more and more studies on how cells that secrete aldosterone increase their aldosterone secretion, and thus increase blood pressure. The electrical charge of the membranes in the cell is the key factor. This charge is determined by the potassium sodium ratio inside and outside the cell. When the charge cannot be maintained at an appropriate level, aldosterone secretion is affected.

Studies of the genes that cause increased aldosterone secretion are consistently showing how critical the potassium channels are. These channels are critical to maintaining the proper level of potassium inside cellular compartments. The proper level of potassium is critical to maintaining correct electrical charges throughout the cell. When potassium is genetically prevented from maintaining a proper level inside aldosterone secreting cells, hypertension results.

More common than this genetic prevention of potassium balance is dietary prevention of potassium balance. Too little potassium (or too much sodium) in the diet will mean that there will be too little potassium inside the cell. This will lead to improper electrical charges throughout the cell. No matter what causes these improper electrical charges, the result will be the same as occurs with the genetic changes. Aldosterone will be affected. Hypertension and organ damage will result.

Food Tables

To find links to tables of the amounts of potassium and sodium in various foods, click on the List Of Posts tab at the top of the page.
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1. Regulation of aldosterone secretion: from physiology to disease. Beuschlein F. Eur J Endocrinol. 2013 Apr 24;168(6):R85-93. doi: 10.1530/EJE-13-0263. Print 2013 Jun.

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Recommended

Two excellent books about high potassium foods and blood pressure reduction are available on Amazon. The first is a practical guide to changing your diet to a high potassium foods diet. It is helpful even if you do not have hypertension. The second is a scientific explanation of the diet. It discusses the changes to your body that occur with high potassium foods.

Practical Guide

Scientific Explanation

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