Researchers have found a link between zinc, blood pressure and kidney sodium transporter in the study of a mouse. These findings, published in the American Journal of Physiology-Renal Physiology, could help researchers design new methods of intervening in at-risk patients.
Zinc is present in cells throughout the body and is needed for the body’s immune system to work properly. It plays a vital role in cell growth, cell division, wound healing, and the carbohydrates breakdown. It is also required for the senses of smell and taste.
Zinc deficiency contributes to high blood pressure
Lower-than-normal zinc levels may cause high blood pressure by altering the way the kidneys handle sodium. Zinc deficiency is very common in individuals with chronic diseases like type 2 diabetes and chronic kidney disease. People with low levels of zinc are also at a higher risk for hypertension. Researchers are still not clear whether levels of zinc are a cause or an effect of higher blood pressure.
The pathway through which the kidneys are involved in either excretion of sodium into the urine or its reabsorption into the body is called the sodium chloride cotransporter (NCC). This pathway also plays a role in blood pressure control.
Low levels of sodium in the urine typically correspond with higher blood pressure. Current research has proposed that zinc may help regulate proteins which in turn regulate the NCC. But a direct connection between zinc-deficiency-induced hypertension has not been observed.
Findings of the study
In this study, the researchers ran a series of trials to examine the relationship between hypertension and zinc, and observe the NCC role.
Researchers compared zinc deficient male mice to healthy controls having normal levels of zinc. They found that the zinc-deficient mice developed high blood pressure and a corresponding reduction in urinary sodium excretion.
However, the control group with normal zinc levels did not experience the same changes. A small group of the zinc-deficient mice was also fed a zinc-rich diet partly through the study.
It was observed that once the levels of zinc reached adequate levels in animals, their blood pressure began to drop and levels of urinary sodium increased.
According to the researchers, these significant results reveal that enhanced renal sodium reabsorption plays a very important role in zinc-deficiency-induced hypertension.
Hence, by understanding the mechanisms through which zinc deficiency contributes to hypertension dysregulation may have an important effect on its treatment in chronic disease settings.