Division of Cardiology, Foundation for Medical Researches, University Hospital, Geneva, Switzerland.
J Nephrol. 2011 Jan-Feb;24(1):23-34. doi: 10.5301/jn.2010.4729.
In spite of the huge amount of research recently performed in this area, the pathogenesis of human hypertension remains elusive. Thus, hypertension has to be defined as "essential" for the majority of patients with high blood pressure. Given the lack of animal models useful to investigate essential hypertension, we analyze and discuss both clinical and basic research studies indicating that essential hypertension should be considered as a potential multifactorial inflammatory disease. The pathophysiology of essential hypertension might result from interactions between genetic and environmental factors. Morphological abnormalities in the renal parenchyma and arteries have also been shown to determine hypertension. Inflammatory processes might induce renal vasoconstriction, ischemia and injury that can sustain systemic hypertension. Arterial and tubulointerstitial infiltration of inflammatory cells in response to renal damage might further increase renal and vascular alterations through the production of oxidants and other soluble inflammatory mediators. The present review gives an update regarding the latest research on the possible direct role of inflammation in the pathophysiology of essential hypertension.
尽管最近在这一领域进行了大量研究，但人类高血压的发病机制仍然难以捉摸。因此，对于大多数高血压患者来说，高血压必须被定义为“原发性”。鉴于缺乏有用的动物模型来研究原发性高血压，我们分析和讨论了表明原发性高血压应被视为一种潜在的多因素炎症性疾病的临床和基础研究。原发性高血压的病理生理学可能是由遗传和环境因素相互作用的结果。肾实质和动脉的形态异常也被证明可以导致高血压。炎症过程可能引起肾血管收缩、缺血和损伤，从而维持全身高血压。炎症细胞在肾损伤后的动脉和小管间质浸润可能通过产生氧化剂和其他可溶性炎症介质进一步增加肾和血管的改变。本综述介绍了炎症在原发性高血压病理生理学中可能直接作用的最新研究进展。
