Sympathetic stimulation through a-receptor causes coronary vasoconstriction, whereas stimulation of (3 receptors causes coronary vasodilatation.
Since the norepinephrine released from sympathetic fibers acts predominantly on receptors, sympathetic stimulation causes coronary vasoconstriction. However, sympathetic stimulation of the heart increases its oxygen demand and the metabolites produced causes coronary vasodilatation.
This indirect (metabolic) vasodilatory effect overrides the direct vasoconstrictive effect (through adrenergic receptors) so that the net effect in vivo is vasodilatation.
Parasympathetic stimulation has variable effects due to its multiple modes of action.
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It tends to cause vasoconstriction because:
(i) it slows down the heart and reduces its oxygen demand;
(ii) the acetylcholine released from parasympathetic fibers acts directly on muscarinic receptors on vascular smooth muscles to produce vasoconstriction.
On the other hand, parasympathetic stimulation tends to cause vasodilatation because:
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(i) the acetylcholine released acts on sympathetic nerve varicosities to inhibit norepinephrine release;
(ii) acetylcholine acts on the endothelium, inducing nitric oxide (NO) release and
(iii) the vasoactive intestinal polypeptide (VIP) co-released with acetylcholine exerts a significant vasodilator effect.