Genetics are involved in hypertension. There are a few conditions that only require the presence of one gene to result in hypertension. These are very rare. Most of the hypertensive genes require multiple factors to result in hypertension. Some of these factors may be multiple other genes. Some may be environmental factors such as food or exercise. A recent review (1) looked at 130 genes that are commonly associated with hypertension.
In the article, the authors refer to hypertension as essential hypertension. This is a term that is still commonly used, but it is an old term that should be abandoned in favor of the term primary hypertension. There is nothing essential about hypertension.
Although somewhat technical, the study is the most up-to-date review concerning genetic and epigenetic changes associated with hypertension. It does not review those hypertensive genes that are monogenic. These are genes that have a change in just one gene causing hypertension. They are extremely rare.
This was a review article that compiled many other articles that were Genome Wide Association Studies (GWAS). Such studies look at thousands of genes at a time to find genes that occur more often in people with a particular disease than people who do not have the disease. In this particular case, they compiled GWA studies that found associations between genes and hypertension.
The study found that the hypertensive genes had multifactorial inheritance. None of those studied had Mendelian inheritance (like blue eyes, brown eyes). The authors found none of the extremely rare genes leading to monogenic hypertension.
They were able to come up with a list of 130 hypertensive genes. Not all of the genes had known functions. However of those with known functions, a great many involved sodium and potassium, either directly or indirectly.
To see what functions were involved was very interesting. Many of them involved the RAAS pathway. This is the pathway that involves hormones affecting blood pressure. Also many of the genes were those affecting how the kidney handles sodium and potassium. At the cellular level, many genes affected the potassium channels, the sodium channels, and the calcium channels one way or another. And many genes involved enzymes associated with balancing potassium and sodium.
The authors also considered epigenetic changes. Epigenetic changes are changes in gene expression caused by mechanisms other than changes in the DNA sequence itself. These are changes such as microRNA, methylation of specific genes or changes in histones (proteins associated with DNA).
This is a more recent area of study that is less developed, so there were fewer studies. Nonetheless, the researchers found some epigenetic overlap with genes affecting potassium and sodium balance. And they also found epigenetic changes influencing genes involved with the results of potassium sodium imbalance, such as nitric oxide and fibrosis.
The authors did emphasize that there was much yet to be discovered and there was no clear set of genetic pathways evident yet. Their hope was that knowing the various genes involved would allow for better design of medications to provide a personal level of prescription.
They felt that discovering genetic pathways would provide little help in determining lifestyle changes. In their view, the lifestyle recommendations to eat better and exercise more would apply to anyone.
However, their study shows that the most common hypertensive genes are highly involved in controlling potassium and sodium. This throws more weight behind specific recommendations concerning potassium and sodium in the diet. When these types of genetic studies are combined with epidemiological and physiological studies, the importance of the potassium sodium ratio in the diet becomes harder to ignore.
The key to controlling blood pressure is controlling the potassium and sodium balance in your body’s cells. This can be done by controlling how much potassium and sodium you get in your diet.
1. Elevated blood pressure: Our family’s fault? The genetics of essential hypertension. Natekar A, Olds RL, Lau MW, Min K, Imoto K, Slavin TP. World J Cardiol. 2014 May 26;6(5):327-37. doi: 10.4330/wjc.v6.i5.327.