Zn deficiency and hypertension

Abstract

Levels of systolic blood pressure (BP) observed immediately before the start of dietary conditioning were significantly higher in spontaneously hypertensive rats (SHR) than in Wistar Kyoto rats (WKY). However, levels of systolic BP and basal mean arterial pressure (MAP) observed at the end of dietary treatment for 4 weeks were SHR fed a Zn-deficient diet > SHR fed a standard diet > WKY fed a standard diet ≒ WKY fed a Zn-deficient diet. Administration of the nitric oxide synthase (NOS) inhibitor, L-NAME caused an increase in MAP levels in SHR fed a standard or a Zn-deficient diet, demonstrating the involvement of the vasodilator, nitric oxide (NO), in the regulation of systemic BP in a genetically hypertensive state. On the other hand, administration of the superoxide scavenger, tempol, led to a decrease in MAP levels in SHR fed a standard or a Zn-deficient diet, indicating the participation of the oxygen free radical, superoxide, in an increase in systemic BP in a genetically hypertensive state. As reported recently, the mechanism involved may be due to a decrease in the action of the vasodilator, NO, based on the formation of peroxynitrite coming from the non-enzymatic reaction of superoxide and NO. In addition, tempol treatment completely restored MAP levels in SHR fed a Zn-deficient diet to levels comparable to those observed in SHR fed a standard diet, indicating that a further increase in systemic BP levels seen in SHR fed a Zn-deficient v.s. a standard diet may be brought by a reduction in the action of the vasodilator, NO, resulting from an increase in superoxide. The activity of the superoxide scavenger, Cu/Zn-superoxide dismutase (SOD), in the thoracic aorta was significantly decreased in SHR fed a Zn-deficient diet relative to SHR fed a standard diet. It appears that a decrease in the activity of Cu/Zn-SOD observed in the thoracic aorta of SHR fed a Zn-deficient diet at least in part plays a role in an increase in superoxide in this model. Thus, Zn deficiency may be a crucial factor to develop genetic hypertension presumably through the oxidative stress caused by superoxide.