Converting-enzyme inhibition prevents aortic collagen accumulation in hypertensive rats via AT1 receptors, and increased aortic stiffness in hypertensive humans is associated with AGTR1 polymorphism.
Does converting-enzyme inhibition or AT1 receptor blockade prevent aortic collagen accumulation and stiffness in hypertension?
This review highlights that the renin-angiotensin system, specifically via AT1 receptors, mediates aortic collagen accumulation and stiffness in hypertension independently of blood pressure changes.
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.
Bénétos et al. (Mon,) conducted a review in Hypertension. Converting-enzyme inhibitors and AT1 receptor blockade was evaluated on Aortic collagen accumulation and aortic stiffness. Converting-enzyme inhibition prevents aortic collagen accumulation in hypertensive rats via AT1 receptors, and increased aortic stiffness in hypertensive humans is associated with AGTR1 polymorphism.