Taddei S, Virdis A, Ghiadoni L, Salvetti A
Cattedra di Medicina Interna, Università degli Studi di Pisa.
Ann Ital Med Int. 1995 Oct;10 Suppl:85S-90S.
In normotensive humans, the endothelium modulates vascular tone mainly by the production of nitric oxide. In human essential hypertension the basal release of nitric oxide is reduced and forearm vasodilation to the endothelium-dependent agonists acetylcholine or bradykinin is blunted. Defective basal release of nitric oxide seems to be secondary to blood pressure increase while impaired agonist-evoked endothelium-dependent vasodilation is probably a primary phenomenon. This latter endothelial dysfunction seems to be caused by the simultaneous presence of an alteration in the L-arginine-nitric oxide pathway and the production of constrictor prostanoids. Defective nitric oxide production is already detectable in normotensive offspring of hypertensive patients and young essential hypertensives. In contrast, vasoconstrictor prostanoid production seems to be associated with aging. In essential hypertensive patients, although only scanty data are available, chronic effective pharmacological treatment seems to restore impaired basal production of nitric oxide but does not improve vascular response to endothelial agonists.
在血压正常的人群中，内皮主要通过产生一氧化氮来调节血管张力。在原发性高血压患者中，一氧化氮的基础释放减少，且前臂对内皮依赖性激动剂乙酰胆碱或缓激肽的血管舒张反应减弱。一氧化氮基础释放缺陷似乎是血压升高的继发结果，而激动剂诱发的内皮依赖性血管舒张受损可能是原发性现象。后一种内皮功能障碍似乎是由L-精氨酸-一氧化氮途径改变和缩血管前列腺素生成同时存在所致。在高血压患者的血压正常后代和年轻原发性高血压患者中，已可检测到一氧化氮生成缺陷。相比之下，缩血管前列腺素的生成似乎与衰老有关。在原发性高血压患者中，尽管仅有少量数据，但长期有效的药物治疗似乎可恢复受损的一氧化氮基础生成，但不能改善血管对内皮激动剂的反应。
