Responses to prostaglandins H2 and I2 of isolated dog cerebral and peripheral arteries

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Abstract
In helical strips of cerebral and peripheral arteries isolated from dogs and contracted with prostaglandin F2 alpha (PGF2 alpha), PGH2 produced a slight transient contraction followed by a relaxation. The relaxation was greater and persisted longer in mesenteric and renal than in cerebral and coronary arteries. Following tranylcypromine or 15-hydroperoxy arachidonic acid, both PGI2 synthetase inhibitors, the relaxation was reversed to a contraction. The contraction was abolished by polyphloretin phosphate, a prostaglandin antagonist. Concentrations of PGI2Na sufficient to produce the same magnitude of relaxations as those induced by PGH2 were greater in mesenteric arteries. PGI2Na or PGI2 methylester caused a dose-related relaxation of the strips contracted with PGF2 alpha or K+, the relaxation being in the order: mesenteric greater than renal greater than coronary greater than cerebral. 6-Keto PGF1 alpha relaxed only mesenteric arteries. It may be concluded that PGH2 is rapidly converted to PGI2 and causes a marked relaxation in dog cerebral and peripheral arteries, the conversion being greater in mesenteric arteries. PGH2, PGE2, and PGF2 alpha all appear to share the same site of excitatory action on arterial smooth muscles. Responses of a variety of isolated dog arteries to vasodilating prostaglandins apparently differ.