Endothelium-dependent收缩。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158846
P M Vanhoutte, T F Lüscher, T Gräser
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引用次数: 106

摘要

内皮细胞通过释放血管活性因子帮助控制下层血管平滑肌的张力。在生理情况下,松弛因子(一氧化氮和内皮源性超极化因子)的释放似乎占主导地位。然而,在某些血管(外周静脉和大脑大动脉)中,正常的内皮细胞有释放血管收缩物质的倾向,其中包括超氧阴离子和血栓素A2;这些内皮来源的血管收缩剂的释放可能有助于自我调节过程。在大多数血管中,缺氧条件启动一种未知的内皮依赖性收缩因子的释放。培养的内皮细胞和在培养条件下长时间维持的血管释放血管收缩肽内皮素。血管疾病的一个特点是内皮细胞释放松弛因子的能力降低,而收缩因子的产生维持或增强。
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Endothelium-dependent contractions.

The endothelial cells help to control the tone of the underlying vascular smooth muscle by releasing vasoactive factors. In physiological circumstances, the release of relaxing factors (nitric oxide and endothelium-derived hyperpolarizing factor) appears to predominate. However, in certain blood vessels (peripheral veins and large cerebral arteries), the normal endothelium has the propensity to release vasoconstrictor substances, among which are superoxide anion and thromboxane A2; the release of these endothelium-derived vasoconstrictors may contribute to the autoregulatory processes. In most blood vessels, anoxic conditions initiate the release of an unidentified endothelium-dependent contracting factor. Cultured endothelial cells, and blood vessels maintained under culture conditions for prolonged periods of time, release the vasoconstrictor peptide endothelin. A characteristic of vascular diseases is that the ability of the endothelial cells to release relaxing factor(s) is reduced, while the generation of contracting factor is maintained or enhanced.

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