The Difference Between Prostaglandin-Mediated Myotropic Effects of Angiotensin Ii and Angiotensin III in the rabbit aorta

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Abstract
The effects of angiotensin II (A II) and its natural metabolic fragment (Des-Asp)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 superfusion medium caused a significant potentiation in the reesponse to A III on the aortic strip. Slight potentiation observed in the response to A II, PG-specific receptor blocker, SC 19220 [1-acetyl-2-(8-chloro-10,11-dihydrodibenz-[b,f][1,4]oxazepine-10-carbonyl)hydrazine] and PG-biosynthesis inhibitor, acetylsalicylic acid, caused a significant inhibition in the response to A III but only acetylsalicylic acid caused a slightly 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. Part of the myotropic effects of A II and A III in rabbit aorta may be mediated through the release of PG. In this respect, A III has higher activity than A II. PG have no role in the myotropic effect of both peptides on the rat colon.