The role of tissue renin-angiotensin system on cardiovascular and renal hypertrophy/hyperplasia

1. 我们评估了三种长效降压药（血管紧张素II受体拮抗剂、ACE抑制剂和钙通道阻滞剂）对慢性肾衰竭（CRF）大鼠的心脏和肾保护作用。结果表明，这些长效降压药对慢性肾功能衰竭大鼠的心脏和肾脏均有保护作用。我们使用ACE抑制剂、一种激肽拮抗剂和一种AII受体拮抗剂，评估了缓动肽-激肽系统介导慢性肾衰竭（CRF）大鼠ACE抑制剂的心脏和肾保护作用的潜力。这些结果表明，在慢性肾功能衰竭大鼠的ACE抑制剂的心脏和肾保护作用中，小钾likrein-kinin系统可能没有发挥主要作用。我们评估了血管紧张素II受体拮抗剂氯沙坦对肾损害糖尿病大鼠的心脏和肾脏的益处。结果表明高血压可加速糖尿病性肾损害，氯沙坦具有抗高血压和保护肾的作用。氯沙坦治疗和卡托普利治疗在减轻心重：体重比增加方面的效力差异可能部分解释了心脏中存在不依赖于血管紧张素转换酶的血管紧张素形成途径。观察氯噻嗪（CTZ）延长治疗左心衰对左冠状动脉结扎所致慢性心肌梗死大鼠心肌肥厚、循环血管活性激素及总可交换体钠（NaE）的影响。CTZ不引起左心衰大鼠心肌肥厚的消退，并激活肾素血管紧张素系统。

1. We assessed the cardio- and reno-protective effects of three kinds of long-acting antihypertensive drugs in rats with chronic renal failure (CRF){an angiotensin II receptor antagonist, an ACE inhibitor, and a calcium channel blocker}. The results indicate that these long-acting antihypertensive drugs equally have the potency to protect heart and kidney in rats with CRF.2. We assessed the potential of the kallikrein-kinin system in mediating the cardio-and reno-protective effects of ACE inhibitors in rats with chronic renal failure (CRF) using ACE inhibitors, a kinin antagonist and an AII receptor antagonist. These results indicate that the kallikrein-kinin system might not play a major role in the cardio-and reno-protective effects of ACE inhibitors in rats with CRF.3. We assessed the cardiac and the renal benefit of an angiotensin II receptor antagonist, losartan, in diabetic rats with renal impairment. The results indicate the hypertension could accelerate diabetic renal impairment and that losartan has antihypertensive and renoprotective effects in this rat model. The difference in potency between losartan treatment and captopril treatment to attenuate the increase in heart weight : body weight ratio might partly explain the existence in the heart of abgiotensin-forming pathways, which are not dependent on angiotensin converting enzyme.4. The effects of prolonged chlorothiazide (CTZ) treatment of left ventricular failure on cardiac hypertrophy, circulating vasoactive hormones and total exchangeable body sodium (NaE) were examined in rats with chronic myocardial infarction induced by left coronary artery ligation. CTZ does not cause regression of cardiac hypertrophy in rats with left ventricular failure and activates the renin angiotensin system.