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pubmed:abstractText |
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 a transient contraction. Both the relaxation and the contraction induced by AII were suppressed by [Sar1,Ala8]AII or [Sar1,Ile8]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 prostaglandin like substance; the release was suppressed by [Sar1,Ala8]AII or indomethacin. It appears that 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.
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