Benetos A, Safar M E
Department of Internal Medicine, Broussais Hospital, Paris, France.
Can J Physiol Pharmacol. 1996 Jul;74(7):862-6.
Converting-enzyme inhibitors decrease the collagen content of the arterial wall in various models of hypertension in rats. Angiotensin II induces collagen production in culture cells. Whether the decrease in collagen induced by converting-enzyme inhibition is due in vivo to pressure mechanisms or to nonhemodynamic factors or a combination of both remains the subject of discussion. In this review, it will be shown that (i) converting-enzyme inhibition prevents the accumulation of aortic collagen in hypertensive rats independently of blood pressure changes, (ii) prevention of aortic collagen accumulation in hypertensive rats is obtained through blockade of angiotensin II formation involving AT1 receptors, and (iii) in hypertensive humans, increased aortic stiffness is associated with AGTR1 receptor polymorphism independently of age and blood pressure.
在大鼠的各种高血压模型中，转换酶抑制剂可降低动脉壁的胶原蛋白含量。血管紧张素II可诱导培养细胞产生胶原蛋白。转换酶抑制所诱导的胶原蛋白减少在体内是由于压力机制、非血流动力学因素还是两者的结合，仍是讨论的主题。在本综述中，将表明：（i）转换酶抑制可独立于血压变化而防止高血压大鼠主动脉胶原蛋白的积累；（ii）通过阻断涉及AT1受体的血管紧张素II形成，可防止高血压大鼠主动脉胶原蛋白的积累；（iii）在高血压患者中，主动脉僵硬度增加与AGTR1受体多态性相关，且独立于年龄和血压。
