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1 We have studied the diuretic and natriuretic effects and the tubular site of action of nifedipine using free water clearance (CH20) and lithium clearance.

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Calcium entry blockers, such as felodipine, increase natriuresis without increasing kaliuresis. Since these drugs acutely increase plasma renin activity without a concomitant change of aldosterone, inhibition of such stimulated aldosterone release might explain the absence of kaliuresis. In a randomized crossover study in 12 male volunteers, we compared the effects of simultaneously administered exogenous aldosterone and felodipine with the effects of either felodipine or aldosterone alone. Felodipine infusion decreased blood pressure, increased renal plasma flow, and induced natriuresis without kaliuresis. Aldosterone alone reduced sodium excretion and increased potassium excretion without influencing hemodynamics. Addition of aldosterone to felodipine attenuated its natriuretic effect and induced a kaliuresis, which clearly exceeded the rise of potassium excretion during aldosterone alone [delta% fractional excretion of K+ +42 +/- 12 with felodipine+aldosterone and +7 +/- 8% with aldosterone alone; means +/- SE, P < 0.02]. Our data suggest that felodipine-mediated inhibition of stimulated aldosterone release is essential for the absence of kaliuresis with felodipine. In addition, the pronounced kaliuresis with aldosterone during felodipine is in keeping with increased distal sodium delivery due to a proximal tubular action of felodipine.

Ten patients with a hypertensive crisis and a decreased renal function were treated with 10 (n =7) or 20 (n=3) mg nifedipine sublingually. Blood pressure was reduced in 60 min from 211 + 4/134 + 5 to 172 + 6/107 ± 6 mm Hg. The decrease of blood pressure was accompanied by a rise in heart rate from 83 ± 6 to 98 ± 5 beats/min. In all seven patients with an encephalopathy signs of this complication were reduced. No serious side-effects were observed.