Renal effects of acute calcium blockade with nifedipine in hypertensive patients receiving beta-adrenoceptor-blocking drugs

Abstract

The effects on blood pressure and renal function of a single 20-mg sublingual dose of nifedipine were investigated in 10 patients with mild to moderate arterial hypertension insufficiently treated on .beta.-blocker monotherapy. Nifedipine induced a prompt and marked reduction of both systolic and diastolic blood pressure (average maximal reduction 30/22 mm Hg, P < 0.001). Despite the .beta.-blockade, heart rate rose 25%. Only insignificant increments of glomerular filtration rate and renal plasma flow were registered, whereas calculated renal vascular resistance (RVR) was markedly reduced (P < 0.001). Urinary excretion rate of albumin and .beta.2 microglobulin rose after nifedipine, reflecting changes in glomerular as well as tubular function. Mean blood pressure seemed to be a major determinant of protein excretion. There was a marked increase in the excretion of Na after nifedipine and urine volume rose from a mean of 8.2 .+-. 1.3 to 12.5 .+-. 1.8 ml/min (P < 0.01). The changes in Na excretion rate correlated with the renal hemodynamic changes. Uric acid excretion rate rose remarkably after nifedipine and the magnitude of the changes seemed intimately related to the basal level of RVR. Nifedipine therapy may be advantageous in patients whose hypertension is insufficiently controlled with .beta.-blockers alone. Renal blood flow is maintained and there is a desirable diuretic action and enhancement of uric acid excretion.