Why doesn't a high potassium foods diet lead to high blood levels of potassium when our kidneys are healthy? Researchers have known for a long time that healthy kidneys can get rid of a lot of potassium in our diets, but the kidneys cannot get rid of much sodium. It has been explained by saying that we have evolved that way. We evolved that way because there was a lot of potassium in the food that prehistoric humans ate and very little sodium. That may be how it came about. But it does not explain the way our bodies do it.
How Our Kidneys Balance Potassium
Recently researchers have figured out the way our bodies do it. We discussed here the recent findings of how normal kidneys can get rid of a lot of potassium, and can recycle sodium. This means that we do not need much sodium in our diet. And since there is no way to get rid of a lot of sodium, we wind up keeping a lot of it in our bodies if we get too much.
One of the requirements for the kidneys to get rid of extra potassium is that the urine produced be alkaline. This was easy for early humans, since the majority of early humans' food contained alkaline precursors that would be excreted in the urine. It is not so easy today because so much of the typical diet lacks these precursors.
Another requirement for excretion of extra potassium is that our bodies produce enough aldosterone. Aldosterone prompts the kidney cells to make the potassium channels needed for excreting potassium into the urine.
How Aldosterone Fits In
Aldosterone is made in the adrenal glands in the area called the zona glomerulosa. When the electric charge (voltage) across the cell membranes of cells in the zona glomerulosa drops (depolarizes), these cells increase their aldosterone production. The aldosterone goes into the blood stream and gets picked up by the kidney cells. Aldosterone in the kidney cells means the kidney cells can make the potassium channels needed to get rid of potassium.
The researchers in this study (1) were looking for a way to study the production of aldosterone in the adrenal gland. Their focus was on the zona glomerulosa, since this is where aldosterone is made. When the voltage across the cell membranes of zona glomerulosa cells drops, more aldosterone is made.
The main two channels affecting the voltage across the cell membranes of the zona glomerulosa cells are the TASK1 and TASK3 potassium channels. They move more potassium across the cell membrane of these cells than any other potassium channels. The researchers sought to find out the effect on aldosterone production from changes in these channels.
The researchers bred some mice that were deficient in these potassium channels. They found that this led to excessive aldosterone production. In the case of mice lacking TASK1, the zona glomerulosa cells made excess aldosterone when the mice were young. After puberty, though, the male mice returned to normal aldosterone production. For mice lacking both TASK1 and TASK3, the production of aldosterone was excessive and remained excessive throughout adulthood.
So the researchers found an excellent model for studying aldosterone production. Aldosterone production depends on the electric charge across the cell membrane of the zona glomerulosa cells. This electric charge (voltage) is determined to a large degree by the potassium channels that cross the cell membrane. If the channels do not function well, the voltage stays too low. This results in aldosterone being chronically secreted, and possibly not be responsive to diet.
When the voltage is low because there is an increase of potassium in the blood stream, the aldosterone produced helps the kidney get rid of the potassium. A diet of high potassium foods will keep the aldosterone production at the right level. And this will keep the blood level of potassium at the right level when the kidney is functioning well. And just like the Yanomami, who have a high aldosterone level because of their high potassium foods diet, you will be protected from hypertension.
1. TASK1 and TASK3 potassium channels: determinants of aldosterone secretion and adrenocortical zonation. Bandulik S, Penton D, Barhanin J, Warth R. Horm Metab Res. 2010 Jun;42(6):450-7. doi: 10.1055/s-0029-1243601. Epub 2010 Jan 4. – links to abstract only