Endothelium-derived hyperpolarizing factor.

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158815
K Komori, P M Vanhoutte
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引用次数: 52

Abstract

Although nitric oxide appears to be the major endothelium-derived relaxing factor (EDRF), it cannot explain all endothelium-dependent responses of isolated arteries. Thus, acetylcholine causes an endothelium-dependent, transient hyperpolarization, which is due to the release from the endothelial cells of a diffusible substance (endothelium-derived hyperpolarizing factor, EDHF) other than nitric oxide. The muscarinic receptors on the endothelium that trigger the release of EDHF belong to the M1-muscarinic subtype, while those activating the liberation of EDRF are M2-muscarinic in nature. The importance of endothelium-dependent hyperpolarization varies among different blood vessels. The hyperpolarization, and the resulting relaxation caused by EDHF can be attributed to an increase in K+ conductance in the vascular smooth muscle. Although the nature of EDHF remains elusive, it may be a labile metabolic of arachidonic acid.

内皮衍生的超极化因子。
虽然一氧化氮似乎是主要的内皮源性松弛因子(EDRF),但它不能解释孤立动脉的所有内皮依赖性反应。因此,乙酰胆碱引起内皮依赖的瞬时超极化,这是由于内皮细胞释放出一种可扩散物质(内皮衍生的超极化因子,EDHF)而不是一氧化氮。内皮上触发EDHF释放的毒蕈碱受体属于m1毒蕈碱亚型,而激活EDRF释放的毒蕈碱受体本质上属于m2毒蕈碱亚型。内皮依赖性超极化的重要性在不同的血管中有所不同。EDHF引起的超极化和由此引起的松弛可归因于血管平滑肌中K+电导的增加。虽然EDHF的性质尚不清楚,但它可能是花生四烯酸的一种不稳定代谢。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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