Regulation of Vascular Smooth Muscle Contraction : The Roles of Ca2+, Protein Kinase C and Myosin Light Chain Phosphatase
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概要
- 論文の詳細を見る
Vasoconstrictors bind to their receptors on the cell surface to activate phospholipase C and Ca2+ channels, resulting in the mobilization of Ca2+ from intracellular are extracellular Ca2+ pools and protein kinase C activation. Vasoconstrictors are also thought to activate a distinct cellular mechanism for downregulating 20kDa myosin light chain (MLC20) phosphatase activity, which involves Rho p21 and protein kinase C, resulting in an increase in the Ca2+ sensitivity of MLC20 phosphorylation. Protein kinase C also appears to activate a MLC20 phosphorylation-independent mechanism for contraction, contributing to the maintenance of agonist-induced contraction. On the other hand, vasorelaxants inhibit activation of phospholipase C and gating of Ca2+ channels, or stimulate Ca2+ extrusion across the plasma membrane, leading to a decrease in the [Ca2+]i. Vasorelaxants also appear to stimulate MLC20 phosphatase activity, resulting in a further reduction of contractile response. The modulatory mechanism for changing the Ca2+ sensitivity, together with the major regulatory mechanism for cellular Ca2+metabolism, plays an important role in regulating vascular smooth muscle tone.
- International Heart Journal刊行会の論文
著者
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Takuwa Yoh
Department Cardiovascular Biology University Of Tokyo
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TAKUWA Yoh
Department of Cardiovascular Biology, Faculty of Medicine, University of Tokyo
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