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Am J Physiol Heart Circ Physiol 264: H665-H669, 1993;
0363-6135/93 $5.00
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AJP - Heart and Circulatory Physiology, Vol 264, Issue 3 665-H669, Copyright © 1993 by American Physiological Society

ARTICLES

M3 and M1 receptors in cerebral arterioles in vivo: evidence for downregulated or ineffective M1 when endothelium is intact

T. Shimizu, W. I. Rosenblum and G. H. Nelson
Department of Pathology (Neuropathology), Virginia Commonwealth University-Medical College of Virginia, Richmond 23298-0017.

Pial arterioles of mice were monitored by intravital television microscopy. Responses to acetylcholine (ACh) and to McN-A-343, a selective M1 activator, were monitored before and after endothelial injury by a laser-dye technique in the presence or absence of different reference antagonists to the M1, M2, and M3 muscarinic receptors. ACh and McN-A-343 produced endothelium-dependent dilation that was blocked by 4-diphenyl-N-methyl-piperidine methiodide, an inhibitor of the M3 receptor. Dilations were not augmented by blocking the M1 receptor with pirenzepine. Endothelial injury unmasked a constricting effect of both ACh and McN-A-343. The constricting effect was blocked by pirenzepine. The results support the literature suggesting an action of McN-A-343 at more than one site. They indicate that ACh causes endothelium-dependent relaxation via the M3 receptor and directly constricts vascular smooth muscle via the M1 receptor. There does not appear to be continuous competition between endothelium-dependent relaxation and endothelium-independent constriction. Rather the M1 receptors mediating constriction in vascular smooth muscle appear downregulated and/or uncoupled from the contractile machinery as long as the overlying endothelium synthesizes/releases the mediator (endothelium-derived relaxing factor) of ACh's dilating action.


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[Abstract] [Full Text] [PDF]


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