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.
Identifer | oai:union.ndltd.org:BSU/oai:cardinalscholar.bsu.edu:handle/180595 |
Date | January 1972 |
Creators | Britton, Steven Loyal |
Contributors | DiSalvo, Joseph |
Source Sets | Ball State University |
Detected Language | English |
Format | vi, 93 leaves : ill. ; 28 cm. |
Source | Virtual Press |
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