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[血管活性内皮因子]

[Vasoactive endothelial factors].

作者信息

Feliciano A, do Rosário H S, Goulão I, Borges M G, Silva M, Rego P, Silvério S, Pedro V

机构信息

Cadeira de Fisiopatologia Geral, Faculdade de Medicina, Lisboa.

出版信息

Rev Port Cardiol. 1993 Jun;12(6):557-60, 510-1.

PMID:8333993
Abstract

Endothelium-derived vasoactive factors are produced by the endothelium activated by effective stimulus, and with paracrine regulatory activity of the tone/proliferation of the vascular smooth muscle and platelet function. They are divided in two groups: endothelium-derived relaxing and contracting factors. Among the endothelium-derived relaxing factors, PG I2, EDRF (NO or other nitrous compound) and EDHF (still unidentified) have been considered Synthetized by the endothelium after stimulation by plasmatic, platelet-derived and endothelium-derived substances and mechanisms, towards the vascular smooth muscle (myorelaxing/cytostatic) and the platelets (antiaggregation). The endothelium-derived contracting factors include the EDCF1 (endothelins, 21 amino acids peptides), EDCF2 (O2-) and TxA2. Its production, induced by stimulus similar to those for relaxing factors, promotes constriction/mitogenesis of the vascular smooth muscle and platelet aggregation. Probably, endothelin-1 has indirect actions over hormonal mechanisms of cardiovascular and renal regulation. The vascular system establishes a tight regulation over the production of these endothelium-derived vasoactive factors. Its loss (usually due to alteration of endothelial responsiveness to stimulation) allows local or generalized modifications of the vascular tone. These can depend on hypertension, atherosclerosis, ischemia-reperfusion lesion, diabetes, inflammation and situations of farmacotoxicity (all developing vasoconstriction/vasospasm) or by septicemia (leading to vasodilation). This disregulation is also involved in the pathogenesis of hypertension, atherosclerosis and ischemia-reperfusion. The vascular tone regulation by endothelium also leads to systemic consequences. Essentially by decreasing cardiac, cerebral and renal blood flow it implies morphologic and functional modifications of these organs.

摘要

内皮源性血管活性因子由有效刺激激活的内皮产生,对血管平滑肌的张力/增殖和血小板功能具有旁分泌调节活性。它们分为两组:内皮源性舒张因子和收缩因子。在内皮源性舒张因子中,前列环素I2、内皮源性舒张因子(一氧化氮或其他含氮化合物)和内皮源性超极化因子(仍未明确)被认为是在受到血浆、血小板源性和内皮源性物质及机制刺激后,由内皮合成,作用于血管平滑肌(舒张/抑制细胞生长)和血小板(抗聚集)。内皮源性收缩因子包括内皮素1(内皮素,21个氨基酸的肽)、内皮源性收缩因子2(超氧阴离子)和血栓素A2。其产生由类似于舒张因子的刺激诱导,促进血管平滑肌的收缩/有丝分裂和血小板聚集。内皮素-1可能对心血管和肾脏调节的激素机制有间接作用。血管系统对这些内皮源性血管活性因子的产生建立了严格的调节。其丧失(通常由于内皮对刺激的反应性改变)会导致血管张力的局部或全身性改变。这些改变可能取决于高血压、动脉粥样硬化、缺血-再灌注损伤、糖尿病、炎症和药物毒性情况(均会导致血管收缩/血管痉挛)或败血症(导致血管舒张)。这种调节异常也参与了高血压、动脉粥样硬化和缺血-再灌注的发病机制。内皮对血管张力的调节也会产生全身性后果。主要通过减少心脏、大脑和肾脏的血流量,这意味着这些器官会发生形态和功能改变。

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