g蛋白与内皮反应。

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158813
N A Flavahan, P M Vanhoutte
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引用次数: 66

摘要

g蛋白是将大量膜结合受体偶联到多种细胞内效应系统的转导蛋白。百日咳毒素adp -核糖基化某些g蛋白,使其功能受到抑制。在猪冠状动脉中,百日咳毒素抑制由α -2-肾上腺素能或血清素能受体刺激以及血小板或凝血酶聚集引起的内皮依赖性松弛。对一氧化氮的松弛和对缓激肽、二磷酸腺苷或A23187的内皮依赖性松弛不受毒素影响。因此,某些内皮依赖性松弛是由内皮细胞中百日咳毒素敏感的g蛋白激活介导的,最有可能是gi蛋白。在再生内皮的猪冠状动脉中(在体内剥落后),百日咳毒素敏感刺激引起的内皮依赖性松弛减少,并且不受百日咳毒素的进一步影响。对其他刺激的松弛不受再生过程的影响,也不受毒素的影响。在再生内皮细胞中,释放EDRF的g蛋白依赖机制可能存在选择性损伤,这可能使血管易发生血管痉挛或引发血管疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
G-proteins and endothelial responses.

G-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely Gi-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to the other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease.

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