RAS阻断与心肾保护.pptVIP

Am. J. Physiol.273 (Heart Circ. Physiol. 42): H1769–H1774, 1997.— 在人心脏中AngII从糜酶产生 糖尿病心肾病变与RAS的特殊关系：  糖尿病脂肪代谢异常导致醛固酮产生 醛固酮又可以促进AT1R 血管紧张素原 血管紧张素1 血管紧张素II 受体（1，2 等） 靶器官作用： 血管收缩 其他非血压依赖作用 肾素 ARB ACEI ACE 糜酶等 结语 心肾结构重塑是高血压的重要后果 RAS过度兴奋是导致心肾结构重塑的重要机制 糖尿病中心、肾病变后果与RAS特别有关 ARB在心肾结构重塑的防治中有特殊作用 Slide 7: Angiotensin II Plays a Central Role in Organ Damage In adult tissues, virtually all known deleterious effects of angiotensin II (A II) ? the end product of the renin-angiotensin system ? are attributable to the AT1 receptor.21 The adverse cerebral and cardiovascular effects of A II, which have potentially lethal sequelae, are pervasive. Preclinical data implicate A II in cerebro-vascular ischaemia through the development of atherosclerosis.22 By potentiating the activity of other neurohormonal systems, A II exerts harmful cardiovascular effects by means of the AT1 receptor 23 ? including vasoconstriction23, vascular hypertrophy 24, left ventricular hypertrophy 24, myocardial and vascular wall fibrosis25, myocardial remodeling24 and cardiac myocyte apoptosis under some conditions25? and thereby contributes to the development of hypertension, heart failure, and myocardial infarction.21,27 A II also plays a central role in the development of renal insufficiency in response to heart failure. As cardiac function deteriorates, decreased renal blood flow leads to a reduced glomerular filtration rate.26 Intense sympathetic activation in heart failure stimulates production of A II in the kidney 26 that initiates a cascade of potentially deleterious renal effects including proteinuria27, increased aldosterone release,21,26 and cell growth and matrix accumulation leading to glomerular sclerosis.28 * * * * 安博维能够有效降低左室重量指数（LVMI）。 Gaudio C等人的一项研究比较了安博维和氨氯地平单药治疗对既往未曾治疗的轻中度高血压患者LVMI的影响，60例患者随机接受安博维或氨氯地平治疗，安博维起始剂量150mg/天，必要时加至300mg；氨氯地平起始剂量5mg/天，必要时加至10mg/天。结果，两组都有50％以上的患者最终接受加倍剂量治疗。研究结果发现，治疗3个月时，安博维治疗组LVMI下降了23.2％，而氨氯地平组只下降了11.4％，两者有显著性差异（ P 0.0001 ）。治疗6个月时，安博维组LVMI下降24.7％，氨氯地平组下降