Although clinical evidence indicates that the autonomic nervous system may be important in initiating coronary artery spasm, the normal neurogenic control of epicardial coronary arteries is poorly understood. Preliminary studies of epicardial canine coronary arteries in vitro indicate that the primary response to norepinephrine released from sympathetic nerves within the blood vessel was is beta-adrenergic dilatation. Worsening of Prinzmetal's angina during treatment with propranolol suggests that inhibition of sympathetic beta-adrenergic vasodilation in human epicardial coronary arteries may result in increased vasoconstrictor tone and lead to vasospasm. The purpose of the proposed studies is to define inhibitory mechanisms which may limit neurogenic beta-adrenergic coronary vascular smooth muscle relaxation. Because parasympathetic cholinergic stimulation is thought to initiate clinical vasospasm, we propose to study prejunctional inhibition of coronary sympathetic beta-adrenergic dilation caused by exogenous acetylcholine and that released by cholinergic nerves. Since platelet aggregation and release of vasoactive substances have been implicated in coronary vasospasm, the inhibitory effects of 5-hydroxytryptamine and aggregating platelets upon neurogenic coronary dilatation and norepinephrine release will also be studied as well blockade of these effects by serotonergic antagonists. Isometric tension of coronary smooth muscle will be studied in vitro. Autonomic newes will be activated by electrical field stimulation. Modulation of norepinephrine release will be studied by measuring overflow of tritiated norepinephrine from coronary arteries preincubated with the tritiated neurotransmitter. Acetylcholine release will be studied following incubation of the tissue with 14C-choline. Possible uptake of 5-hydroxytryptamine by adrenergic nerve terminals will be studied with 14-C-5-hydroxytryptamine.
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