NEUROGENIC CHOLINERGIC PREJUNCTIONAL INHIBITION OF SYMPATHETIC BETA-ADRENERGIC RELAXATION IN THE CANINE CORONARY-ARTERY

  • 1 January 1984
    • journal article
    • research article
    • Vol. 229  (2) , 417-421
Abstract
Electrical stimulation of isolated canine coronary arteries causes release of norepinephrine and subsequent relaxation by activation of .beta. adrenoceptors. This .beta. adrenergic relaxation may be influenced by a concomitant release of acetylcholine. Rings of epicardial coronary arteries of the dog were studied in organ chambers filled with physiological salt solution. The tetrodotoxin-sensitive, .beta. adrenergically mediated relaxation induced by electrical stimulation was studied during contractions evoked by prostaglandin F2.alpha.. The relaxation caused by high-frequency stimulation was not affected by atropine or by removal of the endothelium, indicating that endogenously released acetylcholine does not act directly on the smooth muscle or initiate an endothelium-dependent vasodilator response. In superfused strips of coronary artery preincubated in [3H]norepinephrine, acetylcholine depressed the stimulated overflow of [3H]norepinephrine, indicating prejunctional cholinergic receptors on adrenergic nerve endings. Atropine augmented the overflow, suggesting that endogenous acetylcholine, released during stimulation, inhibits the release of norepinephrine. Evidently, prejunctional inhibition of norepinephrine release, which limits the sympathetic .beta. adrenergic relaxation of the smooth muscle, is the primary neurogenic cholinergic effect in canine epicardial coronary arteries.