Carretero Oscar A
Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202, USA.
J Clin Invest. 2005 Mar;115(3):588-91. doi: 10.1172/JCI24567.
Remodeling of the arterial wall occurs mainly as a consequence of increased wall stress caused by hypertension. In this issue of the JCI, Azizi et al. report that in humans with a kallikrein gene polymorphism that lowers kallikrein activity, the brachial artery undergoes eutrophic inward remodeling in the absence of hypertension or other hemodynamic changes. It has also been reported that alterations of the kallikrein-kinin system are associated with formation of aortic aneurysms. Conversely, after vascular injury, kinins mediate the beneficial effect of angiotensin-converting enzyme inhibitors that prevent neointima formation. These findings raise the intriguing possibility that decreased kallikrein-kinin system activity may play an important role in the pathogenesis of vascular remodeling and disease, while increased activity may have a beneficial effect.
动脉壁重塑主要是由高血压引起的壁应力增加所致。在本期《临床研究杂志》中，阿齐兹等人报告称，在携带降低激肽释放酶活性的激肽释放酶基因多态性的人类中，肱动脉在无高血压或其他血流动力学变化的情况下会发生营养性内向重塑。也有报道称，激肽释放酶-激肽系统的改变与主动脉瘤的形成有关。相反，血管损伤后，激肽介导血管紧张素转换酶抑制剂预防内膜增生的有益作用。这些发现提出了一个有趣的可能性，即激肽释放酶-激肽系统活性降低可能在血管重塑和疾病的发病机制中起重要作用，而活性增加可能具有有益作用。
