The study demonstrates that angiotensin II increases mesenteric vascular resistance while simultaneously stimulating the release of vasodilatory prostaglandins that modulate this pressor response.
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Angiotensin II pressor effects may be prostaglandin-modulated in animal vessels; leaves open relevance to human hypertension mechanisms or therapy.
Isolated Krebs-perfused rabbit-mesentery blood vessels release a prostaglandin E-like substance (PGE) when treated with angiotensin II, angiotensin I, arachidonic acid, or bradykinin. The specific competitive antagonist [Sar1,Ile8]angiotensin II, was found to inhibit angiotensin II-induced PGE release. The angiotensin antagonist did not block PGE release by bradykinin, whereas indomethacin blocked PGE release induced by all agonists. SQ-20881, the converting-enzyme and bradykininase inhibitor, decreased the PGE release by angiotensin I, enhanced the release by bradykinin, and did not affect release by angiotensin II. Pressor and depressor responses were obtained in mesenteric preparations constricted by epinephrine to a pressure of 60 mmHg. Angiotensin II induced an initial increase in mesenteric vascular resistance followed by a depressor response below basal pressure. The pressor responses were enhanced by indomethacin and the depressor responses were eliminated. Bolus injections of both bradykinin and arachidonic acid produced decreases in perfusion pressure, but indomethacin completely inhibited only the arachidonic acid-induced responses while only diminishing bradykinin-induced responses. The ability of angiotensin to increase mesenteric vascular resistance and to release PGE which decrease vascular resistance is discussed.
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Blumberg et al. (1977) studied this question.
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