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In isolated rabbit left atria driven electrically at a frequency of 30/min, the contraction was abolished by increasing external K+ concentrations from 5.4 to 22mM. Addition of isoproterenol (10(-6)M) restored the atrial contraction and the magnitude of contractions increased by raising external concentrations of Ca++ to 4.4 and 6.6. mM. Hexobendine attenuated the magnitude of contractions restored by isoproterenol and excess Ca++ in a dose-dependent manner, as did prenylamine and verapamil. Hexobendine did not significantly influence the membrane depolarization induced by excess K+ and there was no evidence of a beta-adrenergic blocking action. In helical strips of rabbit aortae exposed to Ca++-free media and depolarized by excess K+, the addition of Ca++ caused a marked contraction. Hexobendine, prenylamine and verapamil caused a dose-related attenuation of the Ca++-induced contraction. Relative potencies of the inhibition by hexobendine, prenylamine and verapamil were 1:16.5:100. Inhibitory effects of these drugs were partially antagonized by excess Ca++. Greater attenuation of the contractile response to 25 mM K+ than the response to 2 X 10(-6)M noradrenaline was observed in preparations treated with hexobendine. It may be concluded that interference with the influx of Ca++ across cell membrane in atrial muscles and aortic smooth muscles participates in the inhibition of contractility by hexobendine.

Influence of hexobendine, prenylamine and verapamil on the contractile response of isolated rabbit left atria and aortae to calcium.