Abstract
The effects of angiotensin II (A II) and its natural metabolic fragment (Des-aspartic acid)1-angiotensin II (A III) were studied on the isolated continuously superfused rabbit aortic strip and rat ascending colon. Both peptides induced dose-related myotropic effects on these smooth muscle preparations. Addition of prostaglandin E2 (PGE2) to the super-fusion medium caused a significant potentiation in the response to A III on the aortic strip. However, slight potentiation observed in the response to AII, PG-specific receptor blocker, SC 19220 and PG-biosynthesis inhibitor, acetylsalicylic acid caused a significant inhibition in the response to A III but only acetylsalicylic acid caused a slight inhibition in the response to A II on the aortic strip. Both compounds did not reduce the myotropic effects of the peptides in the rat colon. Addition of PGE2 to the superfusion medium containing acetylsalicylic acid completely prevented the reduced myotropic effects of the peptides. In medium containing acetylsalicylic acid PGE2 produced a highly significant potentiation in the myotropic response of A II on the aorta.These data were taken as evidence that part of the myotropic effects of AII and A III in rabbit aorta are mediated through the release of PG's and in this respect A III has higher activity than A II. However, PG's have no role in the myotropic effect of both peptides on the rat colon.
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