Membrane Electrical Effects of Histamine on Vascular Smooth Muscle of Canine Coronary Artery

Document Type

Article

Publication Date

1-1-1980

Description

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 μm o.d.) 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 mΩ. 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 to 10-5 M). Also, 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+. These findings suggest that histamine increases 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.

Link to Full Text

Share

COinS