Renal hemodynamic effects of a selected calcium antagonist

Abstract

Calcium antagonists are unique antihypertensive drugs that appear to exert selective blood pressure-lowering and possibly renal hemodynamic and functional effects in hypertensive patients and animals. There is evidence for inhibition of tubular sodium reabsorption and renal vasodilatation when certain of these agents are given by acute intravenous or intrarenal arterial administration. These renal effects have been observed to occur either independently or together. Both natriuresis and diuresis have been found to occur with these drugs. In the deoxycorticosterone-salt hypertensive dog, chronically administered diltiazem reduces blood pressure, transiently increases renal blood flow and increases urine volume. Administered either acutely or chronically to these hypertensive dogs, diltiazem depresses renal vascular reactivity. Pressor and renal vasoconstrictor responses to angiotensin II and norepinephrine are attenuated to a similar degree. The chronic blood pressure-lowering effect of diltiazem is most likely a function of depressed vascular reactivity; however, actions at other sites cannot be ruled out based on our experiments. Post-prandial renal vasodilatation readily occurs in the conscious instrumented dog, and although this response is blocked by the acute administration of a calcium antagonist, the response is unaltered during the chronic administration of diltiazem.