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Updated: Aug 27, 2026

Focal Ca2+ Transient Detection in Smooth Muscle
Published on: June 28, 2009
Invited review: mechanisms of calcium handling in smooth muscles
1Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557, USA. kent@physio.unr.edu
Abstract:
The concentration of cytoplasmic Ca(2+) regulates the contractile state of smooth muscle cells and tissues. Elevations in global cytoplasmic Ca(2+) resulting in contraction are accomplished by Ca(2+) entry and release from intracellular stores. Pathways for Ca(2+) entry include dihydropyridine-sensitive and -insensitive Ca(2+) channels and receptor and store-operated nonselective channels permeable to Ca(2+). Intracellular release from the sarcoplasmic reticulum (SR) is accomplished by ryanodine and inositol trisphosphate receptors. The impact of Ca(2+) entry and release on cytoplasmic concentration is modulated by Ca(2+) reuptake into the SR, uptake into mitochondria, and extrusion into the extracellular solution. Highly localized Ca(2+) transients (i.e., sparks and puffs) regulate ionic conductances in the plasma membrane, which can provide feedback to cell excitability and affect Ca(2+) entry. This short review describes the major transport mechanisms and compartments that are utilized for Ca(2+) handling in smooth muscles.
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