Membrane electrical effects of histamine on vascular smooth muscle of canine coronary artery.

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Abstract
This study was undertaken to determine some of the electrophysiological effects of histamine on the coronary arterial vascular smooth muscle of the dog. Transmembrane potentials were recorded from small (< 500 .mu.m o.d. [outer diameter]) isolated canine coronary arteries with glass microelectrodes filled with 3 M KCl. Histamine (10-6 M) increased the resting membrane potential (Em) from -55 to -64 mV and reduced input resistance from 9.8 to 4.0 m.OMEGA.. These effects of histamine were abolished when Mn2+ (1 mM) was added to block Ca2+ influx. The amplitude, maximal rate of rise and frequency of the Ca2+ dependent action potential induced by tetraethylammonium ion (TEA) increased in the presence of histamine in a dose-dependent manner (10-7-10-5 M). The effect of histamine on the TEA-induced action potential was inhibited by the H1 antagonist pyrilamine maleate (10-7 M). When tension was recorded from helically cut strips of coronary arteries, variable results were obtained upon addition of histamine; i.e., some preparations showed no change in tension and others, a small increase. When histamine was added to this preparation in the presence of TEA, tension increased to 60% of the maximum contraction induced by K+. Histamine may increase the Ca2+ inward current in coronary arterial smooth muscle. The hyperpolarization induced by histamine may be due to an increased K+ conductance that is mediated by an increased Ca2+ influx, since inhibition of Ca2+ influx by Mn2+ prevented the hyperpolarization.