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Nonneurogenic relaxation to field stimulation in coronary arteries

S Kalsner and M Quillan

Department of Physiology, City University of New York Medical School, City College of New York.

Coronary artery strips of cattle hearts in vitro respond to transmural stimulation with two potent but distinctly different responses. A neurogenic constriction, attributable to the endogenous release of acetylcholine, is predominant under conditions of minimal and moderate tone. During a high degree of spontaneous tone, and in the presence of near maximal contractions induced by 5-hydroxytryptamine, the response to field stimulation is relaxation rather than constriction. This process was studied more clearly after blockade of the cholinergic effects with atropine. The relaxation response elicited by 5 Hz stimulation for 2 min consisted of two components, one occurring during stimulation and the other promptly after its cessation. The overall relaxation was sufficient to almost obliterate a spontaneous contraction or a near-maximal contraction to 5-hydroxytryptamine. The relaxation to transmural stimulation was unaltered by tetrodotoxin, adrenergic blockade, indomethacin or 5 days cold storage of tissue. Relaxation was elicitable even by a single pulse. With a few pulses, the maximal effect was achieved at 0.5 Hz. Repeated application of three pulses, in strips with spontaneous tone, led to substantial but transient relaxations, which simulated spontaneous rhythm. Removal of the endothelium was without effect on the relaxations, and they were unaltered by inhibition of guanylate cyclase. In the presence of elevated potassium (30 mM), contractions to 5-hydroxytryptamine and those generated spontaneously did not relax to field stimulation. Inhibition of Na+-K+-ATPase with ouabain (5 microM) partially antagonized both components of the relaxation response.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume 250, Issue 2, pp. 461-469, 08/01/1989
Copyright © 1989 by American Society for Pharmacology and Experimental Therapeutics







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Copyright © 1989 by the American Society for Pharmacology and Experimental Therapeutics.