title: [Mechanisms of impairment of endothelial cell].
abstract: 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.
authors.affiliation: Department of Cardiovascular Regeneration and Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University.
authors.forename: Yukihito
authors.initials: Y
authors.lastname: Higashi
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D000804:Angiotensin II; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III