Inhibition of angiotensin conversion in experimental renovascular hypertension.

Abstract

Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normnal in the early phase of renovascular hypertension. These results offer strong evidence that the renin-angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.

• Authors: E D Miller Jr, A I Samuels, E Haber, A C Barger
• Journal: Science (New York, N.Y.) (Science) Vol. 177 Issue 4054 Pg. 1108-9 (Sep 22 1972) ISSN: 0036-8075 [Print] United States
• PMID: 4341125 (Publication Type: Journal Article)

Chemical References

• Peptides
• Venoms
• Angiotensin II
• Renin
• Bradykinin

Topics

• Angiotensin II (metabolism)
• Animals
• Blood Pressure (drug effects)
• Bradykinin (blood)
• Dogs
• Hypertension, Renal (metabolism)
• Injections, Intravenous
• Male
• Peptides (administration & dosage, isolation & purification, pharmacology)
• Renin (blood)
• Venoms (analysis)