Higashi Yukihito
Department of Cardiovascular Regeneration and Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University.
Nihon Rinsho. 2012 Sep;70(9):1519-23.
Nitric oxide (NO) released from endothelial cell plays an important role in the regulation of vascular tone, the inhibition of platelet aggregation, and the suppression of smooth muscle cell proliferation. Activation of renin-angiotensin-aldosterone system(RAAS) plays an important role in the pathogenesis, development, and maintenance of atherosclerosis through an impairment of endothelial function. Angiotensin II stimulates the production of reactive oxygen species by the activation of NADPH oxidase and increases Rho-associated kinase activity that decreases the stability of endothelial nitric oxide synthase (eNOS) mRNA and phosphorylation of eNOS, leading to inactivation of NO bioavailability. An imbalance of reduced production of NO or increased production of reactive oxygen species may promote endothelial cell dysfunction through angiotensin II-induced various signal transduction cascades.
内皮细胞释放的一氧化氮（NO）在调节血管张力、抑制血小板聚集以及抑制平滑肌细胞增殖方面发挥着重要作用。肾素-血管紧张素-醛固酮系统（RAAS）的激活通过损害内皮功能在动脉粥样硬化的发病机制、发展和维持过程中起重要作用。血管紧张素II通过激活NADPH氧化酶刺激活性氧的产生，并增加Rho相关激酶活性，这会降低内皮型一氧化氮合酶（eNOS）mRNA的稳定性以及eNOS的磷酸化，导致NO生物利用度失活。NO生成减少或活性氧生成增加的失衡可能通过血管紧张素II诱导的各种信号转导级联反应促进内皮细胞功能障碍。
