The links between cellular Ca2+ and Na+/H+ exchange in the pathophysiology of essential hypertension

被引：26

作者：

Aviv, A

机构：

[1] Hypertension Research Program, Univ. of Med. and Dent. of New J., New Jersey Medical School, Newark, NJ

[2] Univ. of Med. and Dent. of New J., New Jersey Medical School, Hypertension Res. Program, Newark, NJ 07103-2714

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1996年 / 9卷 / 07期

关键词：

calcium; sodium-hydrogen exchanger; pH; calmodulin; serine/theorine kinase; hypertension;

D O I：

10.1016/0895-7061(95)00447-5

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

This review focuses on the mechanisms whereby the cytosolic Ca2+ regulates the ubiquitous Na+/H+ exchanger (NHE-1) and how these regulatory processes might modify the behavior of NHE-1 in essential hypertension. The pH setpoint for activation of the Na+/H+ exchanger is controlled by two interrelated and Ca2+-dependent pathways, namely, the protein kinase/phosphatase cascade and Ca2+/calmodulin. The cytoplasmic domain of NHE-1 contains elements responsive to serine/theorine kinases and a high affinity binding site to Ca2+/calmodulin. Phosphorylation of NHE-1 or the binding of the Ca2+/calmodulin complex to its binding site promotes an alkaline shift in the pH setpoint for the exchanger. It is suggested that, in essential hypertension, an increased cellular Ca2+ load or an enhanced external Ca2+ entry stimulate the NHE-1 through protein kinase/phosphatase and Ca2+/calmodulin systems, thereby increasing its activity.

引用

页码：703 / 707

页数：5

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