López-Farré A, Farré J, Sánchez de Miguel L, Romero J, González-Fernández F, Casado S
Laboratorio de Nefrología, Hipertensión e Investigación Cardiovascular, Fundación Jiménez Díaz, Madrid.
Rev Esp Cardiol. 1998;51 Suppl 6:18-22.
The endothelium is a dynamic organ involved in the genesis and development of the cardiovascular diseases. Nitric oxide (NO) is one of the factors released from endothelium. NO is generated by endothelial cells through the activity of a constitutive nitric oxide synthase (cNOS). Smooth muscle cells generate NO by an inducible NOS isoform (iNOS). NO regulates vascular tone, different mechanisms involved in the interaction of blood cells to the vascular wall, the growth of smooth muscle cells and the matrix protein synthesis. The lack of an endothelium-dependent vasodilatory response has been defined as endothelial dysfunction. It has been demonstrated a reduced endothelium-dependent vasodilation response in hypertension, aging, atherosclerosis ... and in patients without evident coronary disease. Although the cNOS has been initially described as constitutive, in recent years it has been demonstrated that several pathophysiological stimuli such as hypoxia, chronic exercise, cytokines regulate its level of expression. Our laboratory has demonstrated that an endothelial cytosolic protein regulates the half-lives of eNOS mRNA. This endothelial cytosolic protein could be a target for specific drugs to prevent endothelial dysfunction.
内皮是一个参与心血管疾病发生和发展的动态器官。一氧化氮（NO）是内皮释放的因子之一。内皮细胞通过组成型一氧化氮合酶（cNOS）的活性产生NO。平滑肌细胞通过诱导型NOS同工型（iNOS）产生NO。NO调节血管张力、血细胞与血管壁相互作用所涉及的不同机制、平滑肌细胞的生长以及基质蛋白合成。内皮依赖性血管舒张反应的缺乏被定义为内皮功能障碍。在高血压、衰老、动脉粥样硬化……以及无明显冠心病的患者中，已证实内皮依赖性血管舒张反应降低。尽管cNOS最初被描述为组成型的，但近年来已证明，诸如缺氧、长期运动、细胞因子等几种病理生理刺激可调节其表达水平。我们实验室已证明一种内皮细胞溶质蛋白调节eNOS mRNA的半衰期。这种内皮细胞溶质蛋白可能是预防内皮功能障碍的特定药物的靶点。
