Postsynaptic α1- and α2-Adrenergic Mechanisms in Coronary Vasoconstriction

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Abstract
This study examined the relative importance of postsynaptic .alpha.1- and .alpha.2-adrenoceptors in mediating coronary vasoconstriction in open chest dogs in which the left circumflex coronary artery was cannulated and perfused at a constant rate. The cervical vagus nerves and central connections of the stellate ganglia were transsected, and .beta.-adrenergic blockade was produced with propranolol. Coronary vasconstriction occurred in response to intraarterial administration of both the .alpha.1-agonist phenylephrine and the .alpha.2-agonist BHT 933. The response to phenylephrine was partially blocked with prazosin and nearly completely eliminated by yohimbine. The response to BHT 933 was resistant to prazosin, but almost completely blocked by yohimbine. Coronary vasoconstriction produced by norepinephrine was resistant to prazosin, but was blunted by .alpha.2-adrenergic blockade with yohimbine or idazoxan. Prazosin produced some blunting of coronary vasoconstriction in response to small doses of epinephrine, while yohimbine markedly attenuated epinephrine-induced vasoconstriction at all doses used. Measurements of regional myocardial blood flow with radioactive microspheres demonstrated no transmural redistribution of perfusion during vasoconstriction produced by either .alpha.1- or .alpha.2 stimulation. Thus, although stimulation of both .alpha.1- and .alpha.2-adrenoceptors is capable of causing coronary vasoconstriction, vasoconstriction in response to norepinephrine and epinephrine is mediated principally by postsynaptic .alpha.2-adrenoceptors.