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- PMID: 21709182
- UKPMCID: 21709182
- DOI: 10.1101/cshperspect.a004549
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Calcium signaling in smooth muscle.
Hill-Eubanks, David C; Werner, Matthias E; Heppner, Thomas J; Nelson, Mark T
Cold Spring Harbor perspectives in biology. 2011;3(9):a004549.
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Full-text held externally
- PMID: 21709182
- UKPMCID: 21709182
- DOI: 10.1101/cshperspect.a004549
Abstract
Changes in intracellular Ca(2+) are central to the function of smooth muscle, which lines the walls of all hollow organs. These changes take a variety of forms, from sustained, cell-wide increases to temporally varying, localized changes. The nature of the Ca(2+) signal is a reflection of the source of Ca(2+) (extracellular or intracellular) and the molecular entity responsible for generating it. Depending on the specific channel involved and the detection technology employed, extracellular Ca(2+) entry may be detected optically as graded elevations in intracellular Ca(2+), junctional Ca(2+) transients, Ca(2+) flashes, or Ca(2+) sparklets, whereas release of Ca(2+) from intracellular stores may manifest as Ca(2+) sparks, Ca(2+) puffs, or Ca(2+) waves. These diverse Ca(2+) signals collectively regulate a variety of functions. Some functions, such as contractility, are unique to smooth muscle; others are common to other excitable cells (e.g., modulation of membrane potential) and nonexcitable cells (e.g., regulation of gene expression).
Bibliographic metadata
- P01 HL077378, NHLBI NIH HHS, United States
- P20 R016435, PHS HHS, United States
- PG/07/115, British Heart Foundation, United Kingdom
- R01 DK065947, NIDDK NIH HHS, United States
- R01 HL098243, NHLBI NIH HHS, United States
- R01 HL44455, NHLBI NIH HHS, United States
- R37 DK053832-14, NIDDK NIH HHS, United States
- R37DK053832, NIDDK NIH HHS, United States