探讨环AMP和环GMP在平滑肌松弛中的作用机制。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158852
T M Lincoln, T L Cornwell
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引用次数: 206

摘要

环GMP (cGMP)介导多种血管舒张药物和内源性血管舒张物质的松弛作用。环AMP (cAMP)通过β -肾上腺素能激动剂和其他腺苷酸环化酶激活剂介导松弛。这两种第二信使似乎都能降低血管平滑肌细胞内Ca2+的浓度,从而影响松弛。血管平滑肌细胞中cGMP依赖性蛋白激酶的存在是cAMP和cGMP减少Ca2+所必需的,这表明该酶介导两种环核苷酸的放松作用。尽管cgmp依赖性蛋白激酶的特异性底物蛋白在血管平滑肌中尚未被很好地表征,但新的证据表明,Ca2(+)- atp酶被该激酶磷酸化激活,可能是环核苷酸依赖性松弛的作用机制的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Towards an understanding of the mechanism of action of cyclic AMP and cyclic GMP in smooth muscle relaxation.

Cyclic GMP (cGMP) mediates the relaxing action of a variety of vasodilator drugs and endogenous vasodilator substances. Cyclic AMP (cAMP) mediates relaxation by beta-adrenergic agonists as well as other activators of adenylate cyclase. Both second messengers appear to reduce the concentration of intracellular Ca2+ in vascular smooth muscle cells, thus affecting relaxation. The presence of cGMP-dependent protein kinase in vascular smooth muscle cells is required for the reduction of Ca2+ by cAMP and cGMP, suggesting that this enzyme mediates the relaxing effects of both cyclic nucleotides. Although the specific substrate proteins for cGMP-dependent protein kinase are not well characterized in vascular smooth muscle, new evidence indicates that Ca2(+)-ATPase activation by phosphorylation of phospholamban by the kinase may underlie the mechanism of action of cyclic-nucleotide-dependent relaxation.

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