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

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-dihydroxyvitamin 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.

Phosphate as a factor in sodium sensitivity in normal and high renin hypertension.

Disturbed phosphate (PO4) metabolism has been documented in spontaneously hypertensive rats but poorly studied in humans. Twenty-seven drug-free hypertensive subjects were studied on both a 10- and 100-mmol sodium diet. The response of mean arterial pressure to sodium repletion was directly correlated to the response of plasma renin activity (r = 0.540, p = 0.004) and inversely related to the percent response of serum PO4 concentrations. In the sodium-replete state serum PO4 concentration correlated inversely with plasma vitamin D concentration (r = 0.419, p = 0.026), consistent with PO4 acting as a determinate of vitamin D production. The response of serum calcium and plasma vitamin D concentrations to sodium repletion were correlated (r = 0.392, p = 0.043), consistent with serum calcium levels being a dependent variable, but the responses of serum PO4 and vitamin D concentrations were not. This study suggests that PO4 metabolism may be a determinate of blood pressure response to sodium repletion.