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1 Department of Pharmacology, College of Medicine, The University of Vermont, Burlington, Vermont 05405; and 2 Medical Biotechnology Center, University of Maryland Biotechnology Institute, and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201
Local intracellular Ca2+
transients, termed Ca2+ sparks, are caused by the
coordinated opening of a cluster of ryanodine-sensitive Ca2+ release channels in the sarcoplasmic reticulum of
smooth muscle cells. Ca2+ sparks are activated by
Ca2+ entry through dihydropyridine-sensitive
voltage-dependent Ca2+ channels, although the precise
mechanisms of communication of Ca2+ entry to
Ca2+ spark activation are not clear in smooth muscle.
Ca2+ sparks act as a positive-feedback element to increase
smooth muscle contractility, directly by contributing to the global
cytoplasmic Ca2+ concentration
([Ca2+]) and indirectly by increasing
Ca2+ entry through membrane potential depolarization,
caused by activation of Ca2+ spark-activated
Cl
channels. Ca2+ sparks also have a
profound negative-feedback effect on contractility by decreasing
Ca2+ entry through membrane potential hyperpolarization,
caused by activation of large-conductance, Ca2+-sensitive
K+ channels. In this review, the roles of Ca2+
sparks in positive- and negative-feedback regulation of smooth muscle
function are explored. We also propose that frequency and amplitude
modulation of Ca2+ sparks by contractile and relaxant
agents is an important mechanism to regulate smooth muscle function.
ryanodine-sensitive calcium-release channel; voltage-dependent calcium channel; calcium-sensitive potassium channel; calcium-activated chloride channel; sarcoplasmic reticulum
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