Responses of human, monkey and dog coronary arteries in vitro to carbocyclic thromboxane A2 and vasodilators

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Abstract
Carbocyclic thromboxane A2 (cTxA2), a stable analog of TxA2, and prostaglandin (PG) F2.alpha. contracted helical strips of human, monkey and dog coronary arteries in a concentration-dependent manner. Apparent ED50 values for cTxA2 were markedly less (1/58 in humans, 1/373 in monkeys and 1/397 in dogs) than those for PGF2.alpha.. Maximum contractions induced by cTxA2 and PGF2.alpha. relative to those induced by 30 mM K+ were approximately identical in the human and monkey arteries. PGI2 [prostacyclin] caused a concentration-related relaxation in human and dog coronary arteries maximally precontracted with cTxA2 and in human, monkey and dog coronary arteries partially precontracted with PGF2.alpha.. The relaxation response was greatest in the dog arteries and least in the monkey arteries. Contractions induced by cTxA2 or PGF2.alpha. and relaxations induced by PGI2 were selectively antagonized by treatment with diphloretin phosphate. Human coronary artery strips contracted with cTxA2 responded to nitroglycerin with a rapid, transient relaxation and to verapamil with a slowly developing, persistent relaxation, as did monkey and dog coronary artery strips. Thromboxane (Tx) A2 appears to be one of the most potent endogenous vasoconstrictors in human coronary arteries, if cTxA2 acts on TxA2 receptors. Apparently PGI2, nitroglycerin and verapamil are effective vasodilators in human conduit coronary arteries maximally contracted with cTxA2, although the extent and the duration of vasodilation induced by these agents were quite different.

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