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Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557
The concentration of cytoplasmic Ca2+ regulates the contractile state of smooth muscle cells and tissues. Elevations in global cytoplasmic Ca2+ resulting in contraction are accomplished by Ca2+ entry and release from intracellular stores. Pathways for Ca2+ entry include dihydropyridine-sensitive and -insensitive Ca2+ channels and receptor and store-operated nonselective channels permeable to Ca2+. Intracellular release from the sarcoplasmic reticulum (SR) is accomplished by ryanodine and inositol trisphosphate receptors. The impact of Ca2+ entry and release on cytoplasmic concentration is modulated by Ca2+ reuptake into the SR, uptake into mitochondria, and extrusion into the extracellular solution. Highly localized Ca2+ transients (i.e., sparks and puffs) regulate ionic conductances in the plasma membrane, which can provide feedback to cell excitability and affect Ca2+ entry. This short review describes the major transport mechanisms and compartments that are utilized for Ca2+ handling in smooth muscles.
calcium channel; ryanodine receptor; inositol trisphosphate receptor; calcium sparks; capacitative calcium entry
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