Vascular angiotensin converting enzyme in the development of renal hypertension.
The possible role of vascular angiotensin converting enzyme (ACE) is examined in vitro and in vivo. In helically cut strips of arteries isolated from dogs, contractions induced by angiotensin (ANG) I are suppressed by ACE inhibitor or ANG II antagonist. This indicates that vascular ACE contributes to the local formation of ANG II. In two-kidney, one-clip hypertensive rats, plasma-renin activity (PRA) rises rapidly with the elevation of blood pressure, then decreases gradually, despite sustained high blood pressure. Renin activity in the aorta also increases with the development of hypertension and then decreases in parallel with PRA. ACE activity in plasma does not change before or after the unilateral occlusion of the renal artery until after 16 weeks, whereas the enzyme activity in the aorta significantly increases. The conversion rate calculated from the pressor responses, and from the constricting effects of ANG I and ANG II, both in situ and in helically cut strips obtained from chronic hypertensive rats with increased vascular ACE activities, are significantly higher than those obtained from normotensive rats. Vascular ACE, which can effectively produce ANG II from ANG I locally, appears to play an important role in the maintenance of chronic hypertension.
D000803:Angiotensin I / Q000494:pharmacology / Q000502:physiology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D006977:Hypertension, Renal / Q000209:etiology* / Q000503:physiopathology; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D051381:Rats
D000804:Angiotensin II; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A