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- W152060330 abstract "Calcium plays a key role in excitation–contraction coupling in vascular smooth muscle. Vasoconstrictor agents raise the concentration of free calcium in the cytosol, while vasodilators tend to lower calcium or prevent the vasoconstrictor-induced increase. The calcium that mediates contraction derives from two main sources: intracellular stores and the extracellular space. The main intracellular storage site for releasable calcium is the sarcoplasmic reticulum. Release of calcium from these stores can be triggered by inositol 1,4,5-trisphosphate (IP3), which is formed in the cytosol from the breakdown of phosphatidyl inositol (PI), following the binding of an agonist to its receptor on the cell surface. In response to rapid intracellular application of IP3, vascular muscle develops tension with a much shorter latency than when it is activated by rapid extracellular application of phenylephrine. Receptor activation is thus followed, after a delay, by IP3 production, Ca2+ release, and then contraction. It is also possible that Ca2+ entry may be able to trigger the release of stored Ca2+, thereby resulting in a positive feedback loop that might amplify the cytosolic calcium signal. This chapter focuses on the voltage-operated Ca channels that are the primary target of the organic Ca antagonists. These channels also contribute to the vasodilation produced by the organic nitrates and the relatively new class of drugs known as the potassium-channel openers." @default.
- W152060330 created "2016-06-24" @default.
- W152060330 creator A5036979193 @default.
- W152060330 creator A5067607270 @default.
- W152060330 date "1994-01-01" @default.
- W152060330 modified "2023-10-01" @default.
- W152060330 title "Calcium Channels and Vasodilation" @default.
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