Feliciano A, do Rosário H S, Goulão I, Borges M G, Silva M, Rego P, Silvério S, Pedro V
Cadeira de Fisiopatologia Geral, Faculdade de Medicina, Lisboa.
Rev Port Cardiol. 1993 Jun;12(6):557-60, 510-1.
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.
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。
