Inhibition of captopril-induced renin release by angiotensin II

J. H. Mersey, L. Ceballos, S. Swartz

Research output: Contribution to journalArticlepeer-review

Abstract

The angiotensin-converting enzyme inhibitor (CE1) captopril has been shown to elevate plasma renin activity (PRA) and prostaglandin E2 levels, and to lower blood pressure and angiotensin II (AII) levels. Renin is secreted in both active and inactive forms: however, the interrelationship of these forms and responses to captopril are unclear. We proposed to determine if PRA rise induced by captopril is due primarily to release from All inhibition, and if inactive renin is converted to active renin when PRA increases. Seven normal volunteers were given captopril, 50 mg orally, while on a moderately sodium-restricted diet (35 mEq/day). Changes in PRA and total and inactive renin. as well as prostaglandin E2, were measured. Then, on two different occasions, the captopril dose was preceded or followed by infusion of All, to negate changes in All induced by CEI. The dose of All was obtained by dose-response infusion until a minimal increase in blood pressure occurred. Active renin increased with captopril alone, from 8.2 to 48.3 ng/ml/h by 90 min (p < 0.01). All completely blocked the rise in PRA induced by captopril, whether given before or after captopril. Inactive renin did not decline as active renin increased over the 90-min study. Therefore, the PRA rise induced by captopril is mediated through a fall in All levels and loss of feedback on renin-secreting cells. The rise in PRA comes from secretion of active renin rather than conversion from inactive renin.

Original languageEnglish (US)
Pages (from-to)575-579
Number of pages5
JournalJournal of cardiovascular pharmacology
Volume10
Issue number5
DOIs
StatePublished - Nov 1987

Keywords

  • Angiotensin II
  • Captopril
  • Inactive renin
  • Plasma renin activity
  • Prostaglandin E

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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