Relaxant responses to prostaglandin F2 alpha and E2 of isolated human uterine arteries.

We wished to determine the action of prostaglandins (PG) and to analyze pharmacologically the mechanisms of their action in isolated human uterine arteries in special reference to mediators liberated from the endothelium and subendothelial tissues. Helical strips of the human uterine artery with and without the endothelium were suspended in the Ringer-Locke solution for isometric tension recording. The relaxant response to PGF2 alpha was reversed to a contraction by cyclooxygenase inhibitors and suppressed by tranylcypromine, a PGI2 synthase inhibitor, but was not influenced by endothelium denudation. Relaxations induced by PGE2 and beraprost, a PGI2 analogue, were augmented by cyclooxygenase inhibitors and tranylcypromine but were not affected by ONO3708, an antagonist of vasoconstrictor prostanoids, and endothelium denudation. The potentiating effect of indomethacin was observed in the strips both with and without the endothelium and was antagonized by treatment with beraprost. The relaxation caused by PGF2 alpha apparently is mediated by PGI2 released from subendothelial tissues, whereas the PGE2-induced relaxation is due to the direct action on smooth muscle; the action may be eliminated by the basal release of PGI2 from subendothelial tissues.