Neural control: The traditionally accepted regulatory effects of autonomic innervation of epicardial coronary arteries can be summarized as follows: alpha-adrenergic stimulation induces coronary constriction; beta-adrenergic and parasympathetic stimulation induces coronary vasodilation. Recent developments in this field have upheld the above general findings; however, they have revealed differential regional response and sometimes paradoxic response in the presence of coronary artery disease.
Activation of various receptors yields variable response, depending upon the segment of coronary vasculature. For example, stimulation of alpha receptors on epicardial conduit vessels and meta-arterioles with diameter >50 mm causes constriction, whereas it has a vasodilatory effect on coronary arterioles <50 mm in diameter. Since coronary collateral vessels lack alpha-adrenergic receptors, their resistance will not change with alpha adrenergic stimulation.
In the presence of coronary artery disease, parasympathetic stimulation may lead to net coronary constriction, whereas the net effect in absence of coronary atherosclerosis, as noted above, is vasodilatory. The disruption of endothelium associated with atherosclerosis which serves under normal circumstances as the source of EDRF has been cited as a potential explanation. In other words, normal endothelium, when exposed to acetylcholine, releases EDRF and results in vasodilation.