The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Calcium sparks in smooth muscle
Abstract
Local intracellular Ca 2+transients, termed Ca 2+sparks, are caused by the coordinated opening of a cluster of ryanodine-sensitive Ca 2+release channels in the sarcoplasmic reticulum of smooth muscle cells. Ca 2+sparks are activated by Ca 2+entry through dihydropyridine-sensitive voltage-dependent Ca 2+channels, although the precise mechanisms of communication of Ca 2+entry to Ca 2+spark activation are not clear in smooth muscle. Ca 2+sparks act as a positive-feedback element to increase smooth muscle contractility, directly by contributing to the global cytoplasmic Ca 2+concentration ([Ca 2+]) and indirectly by increasing Ca 2+entry through membrane potential depolarization, caused by activation of Ca 2+spark-activated Cl−channels. Ca 2+sparks also have a profound negative-feedback effect on contractility by decreasing Ca 2+entry through membrane potential hyperpolarization, caused by activation of large-conductance, Ca 2+-sensitive K+channels. In this review, the roles of Ca 2+sparks in positive- and negative-feedback regulation of smooth muscle function are explored. We also propose that frequency and amplitude modulation of Ca 2+sparks by contractile and relaxant agents is an important mechanism to regulate smooth muscle function.
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Cites
Primary structure and expression from complementary DNA of skeletal muscle ryanodine receptor
Takeshima, H., Nishimura, S., Matsumoto, T., Ishida, H., Kangawa, K., Minamino, N., Matsuo, H., Ueda, M., Hanaoka, M., Hirose, T., et al. (1989) · Nature · doi:10.1038/339439a0 · Cited by 1,146
Cited by
Mitochondrial reactive oxygen species and Ca 2+ signaling
Camello-Almaraz, C., Gomez-Pinilla, P. J., Pozo, M. J., & Camello, P. J. (2006) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00217.2006 · Cited by 336
Large-conductance, calcium-activated potassium channels: Structural and functional implications
Ghatta, S., Nimmagadda, D., Xu, X., & O'Rourke, S. T. (2006) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2005.10.007 · Cited by 330
Rich, T. C., Fagan, K. A., Tse, T. E., Schaack, J., Cooper, D. M. F., & Karpen, J. W. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.221381398 · Cited by 276
Ca2+-Activated K+Channels: From Protein Complexes to Function
Berkefeld, H., Fakler, B., & Schulte, U. (2010) · Physiological Reviews · doi:10.1152/physrev.00049.2009 · Cited by 274
Ion channel networks in the control of cerebral blood flow
Longden, T. A., Hill-Eubanks, D. C., & Nelson, M. T. (2016) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x15616138 · Cited by 137
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Metadata
- Authors
- Jaggar, J. H., Porter, V. A., Lederer, W. J., & Nelson, M. T.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2000-02-01
- Volume
- 278
- Issue
- 2
- Pages
- C235-C256
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W1884656506
- Cited by
- 652
- References
- 1
- FWCI
- 16.67
- Type
- journal article
- Language
- en
- Open access
- closed
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