A new study demonstrates a link between zinc deficiency and high blood pressure. The findings could help scientists design new ways of intervening in at-risk patient populations.

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Hypertension is incredibly common; understanding how it works is vital.

High blood pressure, or hypertension, is a huge and growing health concern in the United States.

According to the American Heart Association, hypertension affects more than 100 million people in the U.S.

Over recent years, researchers have noted a relationship between lower zinc levels and hypertension.

However, to date, scientists have been unable to pinpoint zinc’s exact role in the development of hypertension.

For instance, individuals with certain conditions, such as type 2 diabetes and chronic kidney disease, commonly have a zinc deficiency and high blood pressure. Scientists are still unclear whether zinc levels are a cause or an effect of elevated blood pressure.

Similarly, other studies have shown that individuals with lower zinc levels are more likely to be hypertensive.

As further evidence of zinc’s involvement in hypertension, rats that are particularly sensitive to salt and readily develop high blood pressure have lower levels of zinc in their blood.

Recently, a group of researchers set out to investigate the links between zinc and blood pressure. They wanted to dig a little deeper into the mechanisms of action. The team published their findings in the American Journal of Physiology–Renal Physiology.

Sodium absorption plays a vital role in moderating blood pressure. The sodium chloride cotransporter (NCC) in the kidney is particularly important. It reabsorbs sodium from the fluid that is destined to become urine and feeds it back into the body.

Generally, lower levels of sodium in the urine correspond with increased blood pressure. In other words, when the NCC is too active, it pumps more sodium back into the body, the urine removes less, and blood pressure rises.

As the authors write, “Renal modulation of urinary sodium excretion is the cornerstone of [blood pressure] control.”

A number of proteins can interact with the NCC to alter the amount of sodium that the body reabsorbs and excretes.

Zinc acts as a cofactor, which means that it influences the activity of a wide range of proteins, including enzymes, transcription factors, and regulatory proteins.

Researchers think that zinc impacts one of the proteins that moderates the NCC, although they have struggled to find evidence for this.

In this latest study, the scientists ran a series of experiments to investigate the relationship between zinc and hypertension, and observe the role of the NCC.

Firstly, they demonstrated that mice that ate a diet with lower levels of zinc developed hypertension. Then, they split these animals into two groups. They fed half of the animals on a diet that contained adequate levels of zinc. As expected, their blood pressure soon returned to normal.

The researchers gave the remaining mice hydrochlorothiazide, a drug that inhibits the NCC. The blood pressure of these animals also returned to normal. This is because the NCC stopped pumping sodium back into the body, which allowed the urine to flush it away.

In other experiments, the researchers worked on animal tissue in the laboratory. They demonstrated that the NCC is responsible for hypertension that is mediated by zinc deficiency.

They also showed that NCC activity is altered by the presence of zinc — specifically, NCC activity increases when zinc is at a lower level. The scientists believe that when zinc is in short supply, the NCC is more stable and therefore able to function for longer.

These results tie together findings from earlier work and confirm the role of zinc in hypertension. The authors write:

Understanding the specific mechanisms by which [zinc deficiency] contributes to [blood pressure] dysregulation may have an important effect on the treatment of hypertension in chronic disease settings.”