Acute effects of nifedipine on renal electrolyte excretion in normal and hypertensive subjects.

The role of renal calcium handling in the hypotensive response to calcium channel blockers has not been investigated previously. The acute vasodilatory effect of calcium channel blockers may be accompanied by changes in renal electrolyte handling that are important in renal electrolyte handling that are important in producing the hypotensive response seen with these agents. Nifedipine has been shown to cause acute and chronic natriuresis and diuresis, which are important in the ability to use nifedipine chronically in essential hypertension. We prospectively investigated the acute effect of 10 mg of nifedipine orally on renal cation handling in normotensive and untreated essential hypertensive subjects during a standard oral water load. At baseline there was no difference between normotensives and hypertensives in serum ionized calcium or magnesium, or in the urinary fractional excretion of these two cations. Oral nifedipine acutely increased the fractional excretion of sodium without changing the fractional excretion of calcium or magnesium. Nifedipine did not alter the serum concentrations of sodium, calcium, or magnesium. Augmented sodium excretion may play a role in the acute hypotensive response to oral nifedipine. The acute hypotensive response does not seem to be caused by altered renal handling of calcium or magnesium. Counterbalancing effects of nifedipine on proximal and distal nephron calcium handling may explain the disassociation of augmented sodium excretion and no net change in calcium excretion.