Iwamoto Takahiro, Kita Satomi, Katsuragi Takeshi
Department of Pharmacology, School of Medicine, Fukuoka University, Jonan-ku, Fukuoka, Japan.
Trends Cardiovasc Med. 2005 Nov;15(8):273-7. doi: 10.1016/j.tcm.2005.08.004.
Hypertension is the most common chronic disease and is the leading risk factor for death caused by stroke, myocardial infarction, and end-stage renal failure. The critical importance of excess salt intake in the pathogenesis of hypertension is widely recognized. However, the molecular mechanisms underlying salt-sensitive hypertension remain obscure. Recent studies using selective Na(+)/Ca(2+) exchanger (NCX) inhibitors and genetically engineered mice provide compelling evidence that salt-sensitive hypertension is triggered by Ca(2+) entry through NCX type 1 (NCX1) in arterial smooth muscle. Cardiotonic steroids, such as endogenous ouabain, which may contribute to the pathogenesis of salt-sensitive hypertension, seem to be necessary for NCX1-mediated hypertension. These findings have enabled us to explain how high salt intake leads to hypertension and further to describe the potential of vascular NCX1 as a new therapeutic or diagnostic target for salt-sensitive hypertension.
高血压是最常见的慢性疾病，是由中风、心肌梗死和终末期肾衰竭导致死亡的主要危险因素。过量盐摄入在高血压发病机制中的关键重要性已得到广泛认可。然而，盐敏感性高血压背后的分子机制仍不清楚。最近使用选择性钠/钙交换器（NCX）抑制剂和基因工程小鼠的研究提供了令人信服的证据，表明盐敏感性高血压是由动脉平滑肌中通过1型NCX（NCX1）的钙内流触发的。强心甾类化合物，如内源性哇巴因，可能在盐敏感性高血压的发病机制中起作用，似乎是NCX1介导的高血压所必需的。这些发现使我们能够解释高盐摄入如何导致高血压，并进一步描述血管NCX1作为盐敏感性高血压新治疗或诊断靶点的潜力。
