Na+/H+ exchanger

M. Kuro-o

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Recent investigations have revealed that an enhancement of Na+/H+ exchange activity is a frequently observed ion transport abnormality in hypertensive patients. To test the hypothesis that increased Na+/H+ exchange causes hypertension, we produced transgenic mice overexpressing Na+/H+ exchanger and analyzed their Na+ metabolism and blood pressure. Urinary excretion of water and Na+ was significantly decreased in transgenic mice and systolic blood pressure was elevated after salt loading. The impaired Na+ excretion suggested that the Na+/H+ exchanger overexpressed in the renal tubules increased Na+ reabsorption, which caused a blood pressure elevation by Na+ retention after excessive salt intake. Our results demonstrate that overexpression of Na+/H+ exchanger can be a genetic factor for salt-sensitive hypertension.

Original languageEnglish (US)
Pages (from-to)607-611
Number of pages5
JournalNippon rinsho. Japanese journal of clinical medicine
Volume54
Issue number3
StatePublished - Mar 1996

Fingerprint

Sodium-Hydrogen Antiporter
Blood Pressure
Salts
Transgenic Mice
Hypertension
Ion Transport
Kidney
Water

Cite this

Na+/H+ exchanger. / Kuro-o, M.

In: Nippon rinsho. Japanese journal of clinical medicine, Vol. 54, No. 3, 03.1996, p. 607-611.

Research output: Contribution to journalArticle

Kuro-o, M 1996, 'Na+/H+ exchanger', Nippon rinsho. Japanese journal of clinical medicine, vol. 54, no. 3, pp. 607-611.
Kuro-o, M. / Na+/H+ exchanger. In: Nippon rinsho. Japanese journal of clinical medicine. 1996 ; Vol. 54, No. 3. pp. 607-611.
@article{7c295f5124264dd983f591cc3cadf443,
title = "Na+/H+ exchanger",
abstract = "Recent investigations have revealed that an enhancement of Na+/H+ exchange activity is a frequently observed ion transport abnormality in hypertensive patients. To test the hypothesis that increased Na+/H+ exchange causes hypertension, we produced transgenic mice overexpressing Na+/H+ exchanger and analyzed their Na+ metabolism and blood pressure. Urinary excretion of water and Na+ was significantly decreased in transgenic mice and systolic blood pressure was elevated after salt loading. The impaired Na+ excretion suggested that the Na+/H+ exchanger overexpressed in the renal tubules increased Na+ reabsorption, which caused a blood pressure elevation by Na+ retention after excessive salt intake. Our results demonstrate that overexpression of Na+/H+ exchanger can be a genetic factor for salt-sensitive hypertension.",
author = "M. Kuro-o",
year = "1996",
month = "3",
language = "English (US)",
volume = "54",
pages = "607--611",
journal = "Nippon rinsho. Japanese journal of clinical medicine",
issn = "0047-1852",
publisher = "Nipponrinsho Co., Inc.",
number = "3",

}

TY - JOUR

T1 - Na+/H+ exchanger

AU - Kuro-o, M.

PY - 1996/3

Y1 - 1996/3

N2 - Recent investigations have revealed that an enhancement of Na+/H+ exchange activity is a frequently observed ion transport abnormality in hypertensive patients. To test the hypothesis that increased Na+/H+ exchange causes hypertension, we produced transgenic mice overexpressing Na+/H+ exchanger and analyzed their Na+ metabolism and blood pressure. Urinary excretion of water and Na+ was significantly decreased in transgenic mice and systolic blood pressure was elevated after salt loading. The impaired Na+ excretion suggested that the Na+/H+ exchanger overexpressed in the renal tubules increased Na+ reabsorption, which caused a blood pressure elevation by Na+ retention after excessive salt intake. Our results demonstrate that overexpression of Na+/H+ exchanger can be a genetic factor for salt-sensitive hypertension.

AB - Recent investigations have revealed that an enhancement of Na+/H+ exchange activity is a frequently observed ion transport abnormality in hypertensive patients. To test the hypothesis that increased Na+/H+ exchange causes hypertension, we produced transgenic mice overexpressing Na+/H+ exchanger and analyzed their Na+ metabolism and blood pressure. Urinary excretion of water and Na+ was significantly decreased in transgenic mice and systolic blood pressure was elevated after salt loading. The impaired Na+ excretion suggested that the Na+/H+ exchanger overexpressed in the renal tubules increased Na+ reabsorption, which caused a blood pressure elevation by Na+ retention after excessive salt intake. Our results demonstrate that overexpression of Na+/H+ exchanger can be a genetic factor for salt-sensitive hypertension.

UR - http://www.scopus.com/inward/record.url?scp=0030090767&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030090767&partnerID=8YFLogxK

M3 - Article

C2 - 8904212

AN - SCOPUS:0030090767

VL - 54

SP - 607

EP - 611

JO - Nippon rinsho. Japanese journal of clinical medicine

JF - Nippon rinsho. Japanese journal of clinical medicine

SN - 0047-1852

IS - 3

ER -