1988Clinical and Experimental Pharmacology and PhysiologyOpen access

ANGIOTENSINS II AND III PREVENT CAPTOPRIL‐INDUCED RENIN RELEASE IN THE RAT

Gerhard Moldenhauer, Martin Smith, R. Di Nicolantonio, A. E. Doyle, Trefor Morgan

Open full text 6 citations

Abstract

1. The effects of exogenous angiotensins II and III (50 pmol/min i.v.) on plasma renin release following captopril injection (5 mg/kg, i.v.) were studied in anaesthetized Sprague-Dawley rats, to determine whether angiotensin II blockade is the major mechanism by which captopril induces renin release. 2. Captopril produced a 12-fold increase in plasma renin concentration compared with saline-injected controls. This was completely reversed by pre-infusion of angiotensin II or III. 3. The fall in blood pressure following captopril treatment was also abolished by angiotensins II and III pre-infusion. Noradrenaline pre-infusion (200-800 ng/min, i.v.) also prevented the captopril-induced hypotension but did not alter the rise in plasma renin. 4. Ureteric ligation did not significantly reduce captopril-induced renin release suggesting that acute changes in sodium excretion or delivery of electrolyte to the macula densa were not involved in renin release. 5. These findings suggest that captopril induces renin release by inhibiting angiotensin II feedback control of renin secretion and that angiotensin III may also modulate renin release.

About this research paper

What this paper is about

1. The effects of exogenous angiotensins II and III (50 pmol/min i.v.) on plasma renin release following captopril injection (5 mg/kg, i.v.) were studied in anaesthetized Sprague-Dawley rats, to determine whether angiotensin II blockade is the major mechanism by which captopril induces renin release. 2. Captopril produced a 12-fold increase in plasma renin concentration compared with saline-injected controls. This was completely reversed by pre-infusion of angiotensin II or III. 3. The fall in blood pressure following captopril treatment was also abolished by angiotensins II and III pre-infusion. Noradrenaline pre-infusion (200-800 ng/min, i.v.) also prevented the captopril-induced hypotension but did not alter the rise in plasma renin. 4. Ureteric ligation did not significantly reduce captopril-induced renin release suggesting that acute changes in sodium excretion or delivery of electrolyte to the macula densa were not involved in renin release. 5. These findings suggest that captopril induces renin release by inhibiting angiotensin II feedback control of renin secretion and that angiotensin III may also modulate renin release.

Why it matters

OpenAlex reports 6 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

1. The effects of exogenous angiotensins II and III (50 pmol/min i.v.) on plasma renin release following captopril injection (5 mg/kg, i.v.) were studied in anaesthetized Sprague-Dawley rats, to determine whether angiotensin II blockade is the major mechanism by which captopril induces renin release. 2. Captopril produced a 12-fold increase in plasma renin concentration compared with saline-injected controls. This was completely reversed by pre-infusion of angiotensin II or III. 3. The fall in blood pressure following captopril treatment was also abolished by angiotensins II and III pre-infusion. Noradrenaline pre-infusion (200-800 ng/min, i.v.) also prevented the captopril-induced hypotension but did not alter the rise in plasma renin. 4. Ureteric ligation did not significantly reduce captopril-induced renin release suggesting that acute changes in sodium excretion or delivery of electrolyte to the macula densa were not involved in renin release. 5. These findings suggest that captopril induces renin release by inhibiting angiotensin II feedback control of renin secretion and that angiotensin III may also modulate renin release.

Key concepts: Captopril, Renin–angiotensin system, Internal medicine, Endocrinology, Chemistry, Plasma renin activity, Macula densa, Angiotensin II

Related papers

Back to paper searchBrowse research topicsOriginal source
ANGIOTENSINS II AND III PREVENT CAPTOPRIL‐INDUCED RENIN RELEASE IN THE RAT — Research Paper | ScholarLens