Na+/Ca2+ exchanger(NCX1) and salt-sensitive hypertension

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 inhibitors and genetically engineered mice provide compelling evidence that salt-sensitive hypertension is triggered by Ca2+ entry through Na+/Ca2+ exchanger type-1 (NCX1) in vascular smooth muscle. Intriguingly, endogenous Na+ pump inhibitors 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.

作 者：

Iwamoto T

刊 名：

日本臨牀 

年，卷(期)：

2006vol.64(no.1) 

分类号：

 

关键词：

Hypertension  Sodium Chloride, Dietary  Sodium-Calcium Exchanger  高血压  氯化钠, 膳食  钠钙交换蛋白

正文语种：

jpn 

基金项目：