Angiotensin conversion in the coronary and hindlamb vasculatures of canines
The effects of angiotensinsI and II on pump-perfusion pressure were examined in the hindlimb vasculature and in the vasculature supplied by the circumflex coronary artery in dogs. In both vasculatures angiotensins I and II caused dosedependent increases in perfusion pressure reflecting directionally similar changes in resistance to blood flow. Responses to angiotensin I were blocked with SQ 20881, a nonapeptide that specifically inhibits conversion of angiotensin I to angiotensin II. In contrast, P-113, a specific anglotensin II antagonist, abolished increases in perfusion pressure produced by angiotensins I and II. These results suggest that increases caused by local administration of angiotensin I in hindlimb or coronary vasculatures are largely ascribable to its enzymatic conversion to angiotensin II. Such conversion appears to occur to the extent of 31% in the hindlimb vasculature, and 26% in the coronary vasculature.