Lower-than-normal levels of zinc — a nutrient that helps the immune system fight off invading bacteria and viruses — may contribute to hypertension, finds a new study on mice.
The study, from the Wright State University in the US, demonstrated that the way in which the kidneys either excrete sodium into the urine or reabsorb it into the body — specifically through a pathway called the sodium chloride cotransporter (NCC) — also plays a role in controlling high blood pressure.
Zinc deficiency is common in people with illnesses such as Type-2 diabetes and chronic kidney disease.
It also showed that less sodium in the urine typically corresponds with higher blood pressure.
Zinc may help regulate proteins that in turn regulate the NCC, the study suggested.
For the study, researchers compared male mice with zinc deficiency to healthy controls with normal zinc levels.
The results, published in the American Journal of Physiology — Renal Physiology, showed that zinc-deficient mice developed high blood pressure and a corresponding decrease in urinary sodium excretion.
However, the control group did not experience the same changes.
A small group of the zinc-deficient mice were fed a zinc-rich diet partway. Once the animals’ zinc reached adequate levels, blood pressure began to drop and urinary sodium levels increased.
"These significant findings demonstrate that enhanced renal (sodium) re-absorption plays a critical role in (zinc-deficiency)-induced hypertension," said Clintoria R. Williams, a researcher from the varsity.
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, the team noted.