The effect of upright tilt on nifedipine-induced natriuresis

Abstract

Calcium channel blockers are antihypertensive agents with diuretic actions. Yet edema occurs in some patients receiving long-term treatment with these drugs. As with other vasodilators, stimulation for fluid retention could result from systemic vasodilation. We speculated that the upright posture could enhance sodium retention. To test this hypothesis, we studied the effect of upright tilt in 10 patients before and after the oral administration of 20 mg nifedipine. Before nifedipine upright tilt caused a 41% drop in the sodium excretion rate, from 0.27±0.04 to 0.16±0.03 meq/min (p<0.05). Fractional sodium excretion decreased by 46%, from 2.4±0.5 to 1.3±0.3% (p<0.01). Urinary volume and renal plasma flow also decreased (p<0.05). Plasma renin activity (PRA) rose by 46% (p<0.005). With the patients in the supine posture nifedipine increased the sodium excretion rate to 0.49±0.09 meq/min (p<0.05). Fractional sodium excretion was 3.1±0.6 meq/min (p=0.2). The natriuresis took place despite a fall in mean blood pressure and a significant rise in PRA (up 115% from prenifedipine supine values, p< 0.005). Renal plasma flow also increased (p<0.01). The upright tilt caused a reversal of the nifedipine-induced natriuresis. The sodium excretion rate dropped to 0.23±0.05 meq/min and fractional sodium excretion to 13±0.2% (both not different from control). This drop in natriuresis occurred while mean blood pressure was at its lowest and PRA was 254% above the initial levels (p<0.005). The glomerular filtration rate and renal plasma flow also dropped to prenifedipine upright values. The upright posture may boost sodium-retaining stimuli arising from calcium antagonist–induced vasodilation. These joint actions may offset the direct natriuretic action of these drugs. © 1992 American Heart Association, Inc.