Interaction of 1, 25-dihydroxyvitamin D and plasma renin activity in high renin essential hypertension

ED Burgess, RG Hawkins… - American Journal of …, 1990 - academic.oup.com
ED Burgess, RG Hawkins, M Watanabe
American Journal of Hypertension, 1990academic.oup.com
Renin secretion by the kidney is inhibited by an increase in free intracellular calcium
concentration. This increase in free intracellular calcium content may be augmented by
serum 1, 25-dihydroxyvitamin D. In 10 subjects with high renin hypertension, an increase in
dietary sodium intake resulted in an increase in urinary calcium excretion (2.5 to 3.4 mmol/L,
P=. 011) and an increase in serum 1, 25-di-hydroxyvitamin D (51.2 to 61.0 pmol/L, P=. 045).
An inverse correlation existed between the change in vitamin D and the change in plasma …
Abstract
Renin secretion by the kidney is inhibited by an increase in free intracellular calcium concentration. This increase in free intracellular calcium content may be augmented by serum 1,25-dihydroxyvitamin D. In 10 subjects with high renin hypertension, an increase in dietary sodium intake resulted in an increase in urinary calcium excretion (2.5 to 3.4 mmol/L, P = .011) and an increase in serum 1,25-di-hydroxyvitamin D (51.2 to 61.0 pmol/L, P = .045). An inverse correlation existed between the change in vitamin D and the change in plasma renin activity (r = —0.765, P = .01). An inverse correlation also existed between the change in plasma renin activity and the change in mean arterial blood pressure (r = -0.757, P = .011). It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. The resultant fall in PRA in part effected the change in blood pressure to the increased sodium intake. Therefore, 1,25-dihydroxyvitamin D may be a mediator in the response of high renin hypertension to increased sodium intake. Am J Hypertens 1990;3:903-905
Oxford University Press