Neurogenic muscarinic vasodilation in the cat. An example of endothelial cell-independent cholinergic relaxation.

Abstract

Nerve-mediated and acetylcholine-induced dilator behavior of feline posterior auricular arteries was studied in vitro. We evaluated the muscarinic nature and endothelial cell-dependence of the vasodilations and attempted to determine if there are inhibitory muscarinic receptors located directly on the smooth muscle cells in this artery. Transmural nerve stimulation of arteries which were pretreated with guanethidine (5 X 10(-6)M) and constricted with prostaglandin F2 alpha (3 X 10(-6)M) caused a frequency-dependent, tetrodotoxin-sensitive relaxation of up to 50% of induced tone. Atropine (10(-7)M) blocked more than 95% of this response at all frequencies. Removal of the endothelium by rubbing the intimal surface did not affect the magnitude of the response, but prolonged it slightly. Neurogenic relaxations in rubbed preparations were atropine-sensitive, although less so than control at higher stimulation frequencies. Relaxation of this artery to the calcium ionophore A23187 was completely endothelial cell-dependent. However, exogenous acetylcholine caused dose-dependent relaxations both in control and rubbed preparations. We conclude that the posterior auricular artery is an example of a blood vessel which has muscarinic receptors located directly on its smooth muscle cells which, when activated by acetylcholine released from perivascular nerves, mediate a smooth muscle cell relaxation. This finding contrasts with models of the vascular smooth muscle cell which indicates an excitatory role for muscarinic receptors.