Inhibition of angiotensin conversion in experimental renovascular hypertension.
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.
D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001920:Bradykinin / Q000097:blood; D004285:Dogs; D006977:Hypertension, Renal / Q000378:metabolism*; D007275:Injections, Intravenous; D008297:Male; D010455:Peptides / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D012083:Renin / Q000097:blood; D014688:Venoms / Q000032:analysis
D010455:Peptides; D014688:Venoms; D000804:Angiotensin II; D012083:Renin; D001920:Bradykinin