Reversal by angiotensins II and III of the effects of converting enzyme inhibition on renal electrolyte excretion in rats.

Experiments were carried out in anaesthetized rats to compare the abilities of angiotensin II (A II) and angiotensin III (A III) to reverse the effects of angiotensin converting enzyme inhibition (Teprotide) on salt and water excretion. In rats infused with Teprotide, significant increases in urine flow and sodium excretion were observed and arterial blood pressure decreased. Addition of A II (10 pmol min-1) to the Teprotide infusion reduced renal excretion of sodium and water to control values and excretion of potassium to below control. Blood pressure increased to a value significantly higher than that during the control period. In a separate group of rats the natriuretic and diuretic effects of Teprotide were reversed by a similar dose of A III (10 pmol min-1). A primarily angiotensin-mediated action is indicated for the renal effects of Teprotide. Although angiotensins II and III appeared to be equipotent in their abilities to reverse the renal responses to Teprotide, A II caused an increase in arterial blood pressure that was not seen with A III. In a third group of rats A II (10 pmol min-1) was added to the Teprotide infusion and an aortic snare located between the renal arteries was tightened to prevent any increase in left renal perfusion pressure. During this period the rate of sodium excretion from the left kidney was significantly lower than from the right kidney. It is concluded that in the absence of any accompanying 'pressure natriuresis' A II is more potent than A III in its ability to reverse the natriuretic action of Teprotide. The elevation of blood pressure to above control values by a dose of A II only just sufficient to reverse the Teprotide-induced natriuresis suggests that the concentration of angiotensin in the kidney is higher than in plasma and supports the concept of an intrarenal renin-angiotensin system. In the rat both A II and A III may affect renal salt and water excretion by a combination of mechanisms involving glomerular, vascular and tubular receptors. The possibility is raised that differential effects of the active angiotensins on these mechanisms may participate in the regulation of sodium excretion.