MOLECULAR MECHANISUMS OF CARDIOVASCULAR REMODELING

肾素-血管紧张素-醛固酮系统（RAAS）在血压的生理调节和心血管器官损伤的病理生理破坏中起重要作用。血管紧张素II（AngII）是RAAS的主要生物介质。血管紧张素II的病理生理作用是由血管紧张素II I型受体介导的，例如对血管平滑肌的血管收缩、醛固酮的分泌、肾近端肾单位中钠的重吸收以及细胞生长和增殖。以及血管硬化和肾小球硬化。此外，这些作用与抑制TGF-β、I型胶原、II型胶原、纤连蛋白的基因表达有关。这些基因的表达是由Ang II I型受体通过激活丝裂原活化蛋白激酶（ERK和JNK）的刺激引起的。血管紧张素转换酶和血管紧张素Ⅱ Ⅰ型受体拮抗剂均能抑制ERK和JNK的激活。

The renin-angiotensin-aldosterone system (RAAS) plays an important role in both the physiological regulation of blood pressure and in the pathophysiological disruption of cardiovascular organ damages. Angiotensin II (Ang II) is the primary biological mediator of the RAAS. Pathophysiological actions of Ang II is mediated by the angiotensin II type I receptor, for examples of vasoconstriction on vascular smooth muscle, secretion of aldosterone, reabsorption of sodium in the renal proximal nephron, and cell growth and proliferation.Treatments of RAAS inhibitors, angiotensin converting enzyme and Ang II type I receptor antagonist, in hypertensive rat models caused prevention effects of hypertension, cardiac hypertrophy, and vascular sclerosis and glomerular sclerosis. In addition, these effects were associated with suppressive gene expressions of TGF-b, collagen type I, collagen type II, fibronectin. These gene expression were caused by the stimulation of Ang II type I receptor through the activation of mitogen-activated protein kinases (ERK and JNK). Both angiotensin converting enzyme and Ang II type I receptor antagonist inhibited the activation of ERK and JNK.