Control of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscle
Am J Physiol Lung Cell Mol Physiol 279: L722-L732, 2000.，-0001，（）：
Tao, Liang, Yu Huang, and Jean-Pierre Bourreau. Control of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscle. Am J Physiol Lung Cell Mol Physiol 279: L722–L732, 2000.—Full muscarinic stimulation in bovine tracheal smooth muscle caused a sustained contraction and increase in intracellular Ca2+ concentration ([Ca2+]i) that was largely resistant to inhibition by nifedipine. Depletion of internal Ca2+ stores with cyclopiazonic acid resulted in an increased efficacy of nifedipine to inhibit this contraction and the associated increase in [Ca2+]i. Thus internal Ca2+ store depletion promoted electromechanical coupling between full muscarinic stimulation and muscle contraction to the detriment of pharmacomechanical coupling. A similar change in coupling mode was induced by ryanodine even when it did not significantly modify the initial transient increase in [Ca2+]i induced by this stimulation, indicating that depletion of internal stores was not necessary to induce the change in excitation-contraction coupling mode. Blockade of the Ca2+-activated K1 channel by tetraethylammonium, charybdotoxin, and iberiotoxin all induced the change in excitation-contraction coupling mode. These results suggest that in this preparation, Ca2+ released from the ryanodine-sensitive Ca2+ store, by activating Ca2+-activated K1 channels, plays a central role in determining the expression of the pharmacomechanical coupling mode between muscarinic excitation and the Ca2+ influx necessary for the maintenance of tone.
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