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

Abraham Aviv

doi:https://doi.org/10.1016/0895-7061(95)00447-5

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

Abraham Aviv

NJMS-Pediatrics-Human Developm

Rutgers, The State University

Research output: Contribution to journal › Review article › peer-review

25 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	703-707
Number of pages	5
Journal	American journal of hypertension
Volume	9
Issue number	7
DOIs	https://doi.org/10.1016/0895-7061(95)00447-5
State	Published - Jul 1996

ASJC Scopus subject areas

Internal Medicine

Keywords

Calcium
calmodulin
hypertension
pH
serine/theorine kinase
sodium-hydrogen exchanger

Access to Document

https://doi.org/10.1016/0895-7061(95)00447-5

Cite this

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

abstract = "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.",

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AB - 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.

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