Inhibition of angiotensin conversion and prevention of renal hypertension

E. D. Miller, A. I. Samuels, E. Haber, A. C. Barger

Research output: Contribution to journalArticle

Abstract

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment wth the nonapeptide Pyr Trp Pro Arg Pro Gln Ile Pro Pro (SQ 20,881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin angiotensin system is responsible for the initiation of renovascular hypertension in the one kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

Original languageEnglish (US)
Pages (from-to)448-453
Number of pages6
JournalAmerican Journal of Physiology
Volume228
Issue number2
StatePublished - Dec 1 1975
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Physiology (medical)

Cite this