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

Abstract

SUMMARY1. 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.2. 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-) 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.3. In a separate group of rats the natriuretic and diuretic effects of Teprotide were reversed by a similar dose ofA III (10 pmol min-'). A primarily angiotensin-mediated action is indicated for the renal effects of Teprotide.4. 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-) 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.5. 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. 6. 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.

Pressor and Renal Effects of Intracerebroventricularly Administered Angiotensins II and III in Rats

“…Our earlier study [16] demonstrated that ICV administration of ANG III induced diuretic and natriuretic effects in conscious rats. Similar renal actions of ANG II and III have been reported when these peptides are given intravenously [17][18][19]. These observations are compatible with the notion that central ANG II and III may be similar to the well-known peripheral ANG peptides playing an important role in the regulation of body fluid and cardiovascular function.…”

Effects of different angiotensins during acute, double blockade of the renin system in conscious dogs

“…First, studies of the actions of ANG III (des-Asp 1 -ANG II) in the rat (29,32) and in anesthetized dogs (11,24) indicate that infusion of ANG III might produce vasoconstriction, sodium retention, and aldosterone release. This response is thought to be similar to ANG II, although not as potent.…”

Angiotensins Ii and Iii Prevent Captopril‐induced Renin Release in the Rat

“…(1975) showed that All and All1 were equipotcnt in their ability to suppress renin release in the dog, while Naftilan and Oparil(1978) found thai A11 was more potent than AIII in suppressing renin release in vitro. In separate studies, A11 and All1 had been shown to be equipotent in their abilities to reverse the natriuretic and diuretic effects of angiotensin converting enzyme inhibition (Harris & Munro 1984). The physiological role of endogenous A111 and its relative potency compared with All in control ofrenin release awaits more detailed dose-response studies.…”

“…1978) have shown that inhibition of renin secretion may be mediated by the macula densa and dependent on presentation of NaCl to the distal tubule (Briggs & Schnermann 1986). Angiotensin converting enLyme inhibitors are natriuretic in the rat (Harris & Munro 1984) and hence may modulate renin release by altering sodium balance. Therefore to examine whether captopril-induced changes in electrolyte excretion are involved in captopril-induced renin release the effect ofcaptopril on renin release from animals whose kidneys have been rendered non-filtering by bilateral ureteric ligation has been examined (Blaine et al 1970;Nascimento et a/.…”