Erythrocyte ion transport and membrane lipid composition in young and adult rats with NO-deficient hypertension

被引:9
作者
Vokurková, M
Dobesová, Z
Pechánová, O
Kunes, J
Zicha, J [1 ]
机构
[1] Acad Sci Czech Republ, Inst Physiol, Ctr Expt Cardiovasc Res, Videnska 1083, CZ-142020 Prague 4, Czech Republic
[2] Slovak Acad Sci, Inst Normal & Pathol Physiol, Bratislava, Slovakia
关键词
nitric oxide; NO synthase inhibition; L-NAME hypertension; sodium leak; potassium leak; Na+; K+-pump; K+-cotransport;
D O I
10.1016/S0024-3205(03)00486-7
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
The aim of our study was to search for abnormalities of sodium and potassium transport in erythrocytes of male Wistar rats subjected to chronic L-NAME treatment (40 mg/kg/day) for 4 weeks either from weaning (4-week-old) or in adulthood (12-week-old). Sodium content, Na+, K+-pump and Na+, K+-cotransport activity, cation leaks as well as membrane cholesterol and phospholipid contents were determined in fresh erythrocytes. Chronic inhibition of NO synthase elicited similar blood pressure rise in both age groups which did not differ in the degree of NO synthase inhibition. No significant ion transport abnormalities were disclosed in erythrocytes of young NO-deficient rats, whereas erythrocyte Na+ content, outward Na+, K+-cotransport and inward Na+ leak were significantly reduced in adult hypertensive animals compared to age-matched controls. It should be noted that the erythrocytes of adult control rats were characterized by higher activity of Na+, K+-pump and Na+, K+-cotransport, increased Na+ and Rb+ leaks and elevated membrane cholesterol content compared to those of young normotensive controls. Increased Na+ leak and elevated membrane cholesterol content but reduced membrane phosholipid content were revealed in erythrocytes of adult hypertensive rats when compared to young hypertensive rats. It can be concluded that young and adult Wistar rats did not differ in the extent of NO synthase inhibition and blood pressure rise elicited by chronic L-NAME treatment. Our results exclude the important participation of classical sodium transport abnormalities in the pathogenesis of this NO-deficient form of experimental hypertension. (C) 2003 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:1637 / 1644
页数:8
相关论文
共 38 条
[1]
DETERMINANTS OF AORTIC CYCLIC GUANOSINE-MONOPHOSPHATE IN HYPERTENSION INDUCED BY CHRONIC INHIBITION OF NITRIC-OXIDE SYNTHASE [J].
ARNAL, JF ;
WARIN, L ;
MICHEL, JB .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (02) :647-652
[2]
CHRONIC BLOCKADE OF NITRIC-OXIDE SYNTHESIS IN THE RAT PRODUCES SYSTEMIC HYPERTENSION AND GLOMERULAR DAMAGE [J].
BAYLIS, C ;
MITRUKA, B ;
DENG, A .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (01) :278-281
[3]
CHOLESTEROL ENRICHMENT INCREASES BASAL AND AGONIST-STIMULATED CALCIUM INFLUX IN RAT VASCULAR SMOOTH-MUSCLE CELLS [J].
BIALECKI, RA ;
TULENKO, TN ;
COLUCCI, WS .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (06) :1894-1900
[4]
RED-CELL SODIUM IN DOCA-SALT HYPERTENSION - A BRATTLEBORO STUDY [J].
BIN TALIB, HK ;
ZICHA, J .
LIFE SCIENCES, 1992, 50 (14) :1021-1030
[5]
ISOLATION OF NITRIC-OXIDE SYNTHETASE, A CALMODULIN-REQUIRING ENZYME [J].
BREDT, DS ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (02) :682-685
[6]
CANESSA M, 1993, J MEMBRANE BIOL, V134, P107
[7]
Canessa M, 1994, Curr Opin Nephrol Hypertens, V3, P511, DOI 10.1097/00041552-199409000-00006
[8]
THE NA-K-CL COTRANSPORT IN ESSENTIAL-HYPERTENSION - CELLULAR FUNCTIONS AND GENETIC ENVIRONMENT INTERACTIONS [J].
CANESSA, ML .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 1989, 25 :S37-S45
[9]
Mechanism of enhanced calcium sensitivity and α2-AR vasoreactivity in chronic NOS inhibition hypertension [J].
Carter, RW ;
Kanagy, NL .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01) :H309-H316
[10]
CLARET M, 1978, J PHYSIOL-LONDON, V274, P247, DOI 10.1113/jphysiol.1978.sp012145