Ca2+ sparks act as potent regulators of excitation-contraction coupling in airway smooth muscle.

The Journal of Biological Chemistry
Ronghua ZhuGeLawrence M Lifshitz

Abstract

Ca2+ sparks are short lived and localized Ca2+ transients resulting from the opening of ryanodine receptors in sarcoplasmic reticulum. These events relax certain types of smooth muscle by activating big conductance Ca2+-activated K+ channels to produce spontaneous transient outward currents (STOCs) and the resultant closure of voltage-dependent Ca2+ channels. But in many smooth muscles from a variety of organs, Ca2+ sparks can additionally activate Ca2+-activated Cl(-) channels to generate spontaneous transient inward current (STICs). To date, the physiological roles of Ca2+ sparks in this latter group of smooth muscle remain elusive. Here, we show that in airway smooth muscle, Ca2+ sparks under physiological conditions, activating STOCs and STICs, induce biphasic membrane potential transients (BiMPTs), leading to membrane potential oscillations. Paradoxically, BiMPTs stabilize the membrane potential by clamping it within a negative range and prevent the generation of action potentials. Moreover, blocking either Ca2+ sparks or hyperpolarization components of BiMPTs activates voltage-dependent Ca2+ channels, resulting in an increase in global [Ca2+](i) and cell contraction. Therefore, Ca2+ sparks in smooth muscle presenting both...Continue Reading

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Citations

Jul 13, 2011·The Journal of General Physiology·Lawrence M LifshitzRonghua ZhuGe
Dec 15, 2012·American Journal of Respiratory and Critical Care Medicine·Cheng-Hai ZhangRonghua ZhuGe
Mar 9, 2013·PLoS Biology·Cheng-Hai ZhangRonghua ZhuGe
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Apr 1, 2014·European Journal of Medicinal Chemistry·Amanda Sánchez-RecillasSamuel Estrada-Soto
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