Department of Medicine, University of Padova, Treviso, Italy.
J Hypertens. 2012 Oct;30(10):1885-93. doi: 10.1097/HJH.0b013e328356c257.
It is now well established that hypertension is accompanied by remodeling of the arterial wall with significant modifications in extracellular matrix composition and in vascular cell phenotype. Some of these changes, particularly elastin fragments generation, increased proteases activity and activation of transforming growth factor-β signaling together with deposition of collagen and proteoglycans might generate a permissive soil for vascular calcification. On the other hand, calcium deposits within large arterial conduits can reduce vessel's elasticity and contribute to the generation of blood pressure pattern associated with vascular stiffness, namely isolated systolic hypertension. Hence, a hypothetical vicious cycle exists between hypertensive arterial damage and vascular calcification. Herein, we revised clinical and basic science findings supporting this possibility.
现在已经证实,高血压伴随着动脉壁的重塑,细胞外基质组成和血管细胞表型发生显著改变。其中一些变化,特别是弹性蛋白片段的生成、蛋白酶活性的增加以及转化生长因子-β信号的激活,以及胶原蛋白和糖胺聚糖的沉积,可能为血管钙化创造了有利条件。另一方面,大的动脉管道内的钙沉积会降低血管的弹性,并导致与血管僵硬相关的血压模式的产生,即单纯收缩期高血压。因此,高血压性动脉损伤和血管钙化之间存在一个假设的恶性循环。本文综述了支持这种可能性的临床和基础科学研究结果。