首页> 外文期刊>The Journal of Physiology >(Sub)family feud: crosstalk between TRPC channels in vascular smooth muscle cells during vasoconstrictor agonist stimulation.
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(Sub)family feud: crosstalk between TRPC channels in vascular smooth muscle cells during vasoconstrictor agonist stimulation.

机译:(子)家庭争执:血管收缩剂激动剂刺激期间血管平滑肌细胞中TRPC通道之间的串扰。

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摘要

Agonist-dependent activation of non-selective cation channels belonging to the canonical (C) transient receptor potential (TRP) subfamily has a profound influence on vascular tone (Inoue et al. 2001) and proliferation (Abramowitz & Birnbaumer, 2009) of arterial myocytes, responses that can contribute to cardiovascular diseases such as hypertension and atherosclerosis. TRPC channels are indirectly sensitive to extracellular substances. Vasoactive molecules binding to specific G-protein-coupled receptors (GPCRs) on the plasma membrane of smooth muscle cells (SMCs) activate intracellular signalling pathways leading to increased influx of Na~+ and Ca~(2+). Cation entry depolarizes the sarcolemma and increases Ca~(2+) influx via voltage-dependent Ca~(2+) channels, thereby elevating myocyte contractility and activating other Ca~(2+)-dependent pathways. TRPC-mediated Ca~(2+) entry may also directly influence SMC function.
机译:属于规范性(C)瞬态受体电位(TRP)亚家族的非选择性阳离子通道的激动剂依赖性激活对动脉肌细胞的血管张力(Inoue等人2001)和增殖(Abramowitz&Birnbaumer,2009)产生深远影响可能导致心血管疾病(例如高血压和动脉粥样硬化)的反应。 TRPC通道对细胞外物质间接敏感。与平滑肌细胞(SMC)质膜上的特定G蛋白偶联受体(GPCR)结合的血管活性分子激活细胞内信号传导途径,导致Na〜+和Ca〜(2+)的流入增加。阳离子的进入使肌膜去极化,并通过依赖电压的Ca〜(2+)通道增加Ca〜(2+)的流入,从而提高了心肌细胞的收缩能力并激活了其他依赖Ca〜(2+)的途径。 TRPC介导的Ca〜(2+)的进入也可能直接影响SMC的功能。

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