Author:
García M. C.,Escamilla-Sánchez J.
Abstract
K+ contractures were elicited in small bundles of tonic skeletal muscle fibres of the frog. Adrenaline (1 μM) increased the amplitude of K+ contractures in a [K+]o-dependent manner: maximal effects were produced between 20 and 60 mM [K+]o. In contrast, we found no effect of adrenaline on K+ contractures of twitch fibres. The potentiating effect of adrenaline depended on [Ca2+]o. Increasing [Ca2+]o from 1.8 to 10 mM doubled the positive inotropic effect of adrenaline. In a nominally Ca2+ free saline, adrenaline had no potentiating effect. The Ca2+ channel blockers nifedipine (20 μM) and Ni2+ (1.8 mM) reversibly reduced the amplitude of the tonic phase of K+ contractures and blocked the potentiation by adrenaline. The mechanical effects of adrenaline cannot be explained by changes in the membrane potential, as revealed by intracellular recordings at several [K+]o. It Was concluded that the potentiating effect of adrenaline in tonic muscle fibres of the frog may be mediated through Ca2+ channels.Key words: adrenaline, slow muscle, excitation–contraction coupling, potassium contractures.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
10 articles.
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