acetylstrophanthidin and cesium-chloride

The electrophysiological effects of insulin were studied in canine false tendons (FT) and papillary muscles from kittens and rats. Insulin caused hyperpolarization (2-8 mV) and an increase in action potential (AP) amplitude. However, the rate of rise and duration of the AP, the slope of phase 4 depolarization and conduction velocity were unchanged in the normal tissues. In preparations depressed spontaneously or by stretch or low pH (6.7), hyperpolarization was larger than observed in normal tissues. Insulin partially normalized electrophysiological parameters under these conditions but not in the presence of anoxia (95% N2). The membrane resistances of normal canine FT and kitten papillary muscles were not changed by insulin. Blockade of K channels by CsCl doubled hyperpolarization induced by the hormone. Insulin effects were abolished by cold (21 degrees C), ouabain (3-9 X 10(-7) M), or acetylstrophanthidin (0.5-3 X 10(-6) M). Overdrive hyperpolarization was enhanced by insulin. These experiments suggest that insulin-induced hyperpolarization is mediated by activation of the electrogenic Na pump and not by a change in membrane conductance.

Topics: Action Potentials; Animals; Cats; Cesium; Chlorides; Cold Temperature; Dogs; Dose-Response Relationship, Drug; Electric Conductivity; Female; Hypoxia; In Vitro Techniques; Insulin; Male; Membrane Potentials; Ouabain; Papillary Muscles; Purkinje Fibers; Rats; Strophanthidin