Abstract
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.