Premium
ANGIOTENSINS II AND III PREVENT CAPTOPRIL‐INDUCED RENIN RELEASE IN THE RAT
Author(s) -
Moldenhauer G. K.,
Smith M. D.,
Nicolantonio R. Di,
Doyle A. E.,
Morgan T. O.
Publication year - 1988
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1988.tb01052.x
Subject(s) - captopril , renin–angiotensin system , medicine , endocrinology , chemistry , plasma renin activity , macula densa , angiotensin ii , saline , pharmacology , blood pressure
SUMMARY 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.