Regulation of vascular smooth muscle contraction. The roles of Ca2+, protein kinase C and myosin light chain phosphatase.

Regulation of vascular smooth muscle contraction. The roles of Ca2+, protein kinase C and myosin light chain phosphatase.
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血管平滑肌收缩的调节。

DOI:
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发表时间:
1996
期刊:
Japanese Heart Journal
影响因子:
--
通讯作者:
Yoh Takuwa
Yoh Takuwa
中科院分区:
--
文献类型:
--
作者:
Yoh Takuwa

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血管收缩剂与细胞表面的受体结合,激活磷脂酶C和Ca2+通道,导致细胞内和细胞外Ca2+池中Ca2+的动员和蛋白激酶C的激活。血管收缩剂也被认为激活了下调20 kDa肌球蛋白轻链(MLC20)磷酸酶活性的独特细胞机制,其中涉及Rho p21和蛋白激酶C,导致MLC20磷酸化的Ca2+敏感性增加。蛋白激酶C似乎也激活了MLC20磷酸化无关的收缩机制,有助于维持激动剂诱导的收缩。另一方面,血管松弛剂抑制磷脂酶C的激活和Ca2+通道的门控,或刺激Ca2+在质膜上的挤压,导致[Ca2+]i的减少。血管松弛剂似乎也刺激MLC20磷酸酶活性,导致收缩反应进一步减少。Ca2+敏感性变化的调节机制与细胞Ca2+代谢的主要调控机制一起,在调节血管平滑肌张力中起重要作用。
Vasoconstrictors bind to their receptors on the cell surface to active 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 20 kDa 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.
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