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Endothelium-dependent contractions: when a good guy turns bad!

机译:内皮依赖性收缩:当一个好男人变坏时!

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摘要

Endothelial cells can induce contractions of the underlying vascular smooth muscle by generating vasoconstrictor prostanoids (endothelium-dependent contracting factor; EDCF). The endothelial COX-1 isoform of cyclooxygenase appears to play the dominant role in the phenomenon. Its activation requires an increase in intracellular Ca2+ concentration. The production of EDCF is inhibited acutely and chronically by nitric oxide (NO), and possibly by endothelium-dependent hyperpolarizing factor (EDHF). The main prostanoids involved in endothelium-dependent contractions appear to be endoperoxides (PGH2) and prostacyclin, which activate thromboxane-prostanoid (TP) receptors of the vascular smooth muscle cells. Oxygen-derived free radicals can facilitate the production and/or the action of EDCF. Endothelium-dependent contractions are exacerbated by ageing, obesity, hypertension and diabetes, and thus are likely to contribute to the endothelial dysfunction observed in older people and in essential hypertensive patients.
机译:内皮细胞可通过产生血管收缩性前列腺素(内皮依赖性收缩因子; EDCF)来诱导潜在的血管平滑肌收缩。环氧合酶的内皮COX-1同工型似乎在该现象中起主要作用。它的激活需要增加细胞内Ca 2 + 的浓度。一氧化氮(NO)可能会急性和长期抑制EDCF的产生,而内皮依赖性超极化因子(EDHF)可能会抑制它。参与内皮依赖性收缩的主要前列腺素似乎是内过氧化物(PGH2)和前列环素,它们激活血管平滑肌细胞的血栓烷-前列腺素(TP)受体。氧衍生的自由基可以促进EDCF的产生和/或作用。衰老,肥胖,高血压和糖尿病会加剧内皮依赖性收缩,因此可能导致老年人和原发性高血压患者的内皮功能障碍。

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