Angiotensin-induced relaxation in isolated dog renal and cerebral arteries

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Abstract
Helically cut strips of dog renal and cerebral (basilar and middle cerebral) arteries contracted with prostaglandin-(PG)-F2.alpha. relaxed in response to angiotensin II (AII; 10-9 to 10-7 M) in a dose-dependent manner. In renal arterial strips the relaxation was preceded by transient contraction. Both the relaxation and the contraction induced by AII were suppressed by [Sar, Ala]AII or [Sar, Ile]AII. Treatment with propranolol, atropine, hexamethonium, cocaine, aminophylline, cimetidine or ouabain failed to alter the relaxing effect of AII. The peptide-induced relaxation was reversed to a contraction by aspirin or indomethacin. Treatment with tranylcypromine or 15-hydroperoxy arachidonic acid suppressed the relaxation induced by AII in renal and cerebral arteries but did not alter relaxations induced by PGI2 or K+ (5 mM). In experiments with superfused dog renal and coronary arteries and rat stomach strips, the renal arteries in response to AII released a prostaglandinlike substance; the release was suppressed by [Sar, Ala]AII or indomethacin. The relaxation of isolated dog renal and cerebral arteries induced by AII is mediated by the release of PGI2 which is associated with stimulation of AII receptors.