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(Hypertension. 1995;25:978-980.)
© 1995 American Heart Association, Inc.

Articles

Na⁺-H⁺ Exchange and Essential Hypertension

A New Approach

John P. Reeves; Abraham Aviv

From the Hypertension Research Center and the Department of Physiology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark.

Correspondence to Dr Abraham Aviv, Hypertension Research Center, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, 185 S Orange Ave, MSB F-464, Newark, NJ 07103-2714.

Key Words: hypertension • phosphorylation • calcium • phenotype • Na⁺-H⁺ exchange

	Introduction

 
Enhanced activity of the ubiquitous (housekeeping) isoform of the Na⁺-H⁺ exchanger (NHE-1) is expressed in circulating cells from a subset of patients with essential hypertension (reviewed in Reference 1¹ ). This results from differences in pathways regulating exchanger function, since no mutations have been shown in the NHE-1 gene in patients with essential hypertension.^{2 3} A 1993 report by Rosskopf et al⁴ demonstrated that this phenotype persisted in immortalized lymphoblasts generated with Epstein-Barr virus from the lymphocytes of patients with essential hypertension. The lymphoblasts from hypertensive patients also showed an increased proliferation rate compared with those from normotensive subjects. Since these cells can be easily obtained from patients and maintained indefinitely in tissue culture, the findings of Rosskopf et al signaled the arrival of a new approach to studying the cellular manifestations of essential hypertension. In this issue of Hypertension, Ng and colleagues⁵ confirm the original findings of Rosskopf et al and provide important clues as to the molecular basis for the elevated NHE-1 activity in essential hypertension. These investigators show that the enhanced exchange activity is caused by an increased turnover of the exchanger itself and that this is associated with an increased phosphorylation of the NHE-1 protein. An additional finding reported by Ng et al is that the increased NHE-1 activity is also expressed in immortalized lymphoblasts from subjects who are normotensive but have a family history of essential hypertension.

There are several technical differences in the study of Ng et al⁵ and the previous study. Rosskopf . . . [Full Text of this Article]

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