Vascular sodium pump:: endothelial modulation and alterations in some pathological processes and aging

被引:46
作者
Marín, J
Redondo, J
机构
[1] Univ Autonoma Madrid, Fac Med, Dept Farmacol & Terapeut, C Arzobispo Morcillo 4, E-28029 Madrid, Spain
[2] Clin Puerta Hierro, Serv Farmacol Clin, Madrid, Spain
关键词
vascular sodium pump; hypertension; diabetes; aging; ouabain-like factors; endothelium;
D O I
10.1016/S0163-7258(99)00037-6
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The vascular Na+ pump maintains intracellular ionic concentration and controls membrane potential. Its inhibition by cardiac glycosides enhances the intracellular Na+ concentration. This in turn activates the Na+-Ca2+ exchange mechanism, which induces intracellular Ca2+ increase, membrane depolarization, and noradrenaline release from perivascular adrenergic nerve endings; mechanisms that promote vasoconstriction. This article reviews the relevance of the Na+ pump in vascular tone regulation and the modulation of its activity by the endothelium, The endothelium negatively modulates the vasoconstriction elicited by Na+ pump inhibition by the release of nitric oxide, according to some authors, or an unknown factor, as suggested by others, The possible existence of endogenous digitalis-like factors is also reviewed, as is the involvement of the vascular Na+ pump in some cardiovascular disorders and aging, (C) 1999 Elsevier Science Inc, FLU rights reserved.
引用
收藏
页码:249 / 271
页数:23
相关论文
共 350 条
[1]   SODIUM-METABOLISM IN RAT RESISTANCE VESSELS [J].
AALKJAER, C ;
MULVANY, MJ .
JOURNAL OF PHYSIOLOGY-LONDON, 1983, 343 (OCT) :105-&
[2]   CONTRACTIONS OF CANINE VASCULAR SMOOTH-MUSCLE CELLS CAUSED BY OUABAIN ARE DUE TO RELEASE OF NOREPINEPHRINE FROM ADRENERGIC-NERVE ENDINGS [J].
AARHUS, LL ;
SHEPHERD, JT ;
TYCE, GM ;
VERBEUREN, TJ ;
VANHOUTTE, PM .
CIRCULATION RESEARCH, 1983, 52 (05) :501-507
[3]   INTERRELATIONSHIP BETWEEN NA-+ AND CA-2+METABOLISM IN HYPERTENSION [J].
ABBOTT, A .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1988, 9 (04) :111-113
[4]   SYMPATHETIC CROSS-INNERVATION OF SHR AND GENETIC-CONTROLS SUGGESTS A TROPHIC INFLUENCE ON VASCULAR MUSCLE MEMBRANES [J].
ABEL, PW ;
HERMSMEYER, K .
CIRCULATION RESEARCH, 1981, 49 (06) :1311-1318
[5]   HIGH-AFFINITY OUABAIN BINDING-SITE AND LOW-DOSE POSITIVE INOTROPIC EFFECT IN RAT MYOCARDIUM [J].
ADAMS, RJ ;
SCHWARTZ, A ;
GRUPP, G ;
GRUPP, I ;
LEE, SW ;
WALLICK, ET ;
POWELL, T ;
TWIST, VW ;
GATHIRAM, P .
NATURE, 1982, 296 (5853) :167-169
[6]   CANINE MESENTERIC-ARTERY NA+,K+-ATPASE - VASOPRESSOR RECEPTOR FOR DIGITALIS [J].
ADAMS, RJ ;
WALLICK, ET ;
ASANO, G ;
DISALVO, J ;
FONDACARO, JD ;
JACOBSON, ED .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1983, 5 (03) :468-482
[7]   DIGITALIS SENSITIVITY OF NA+,K+-ATPASE, MYOCYTES AND THE HEART [J].
AKERA, T ;
NG, YC .
LIFE SCIENCES, 1991, 48 (02) :97-106
[8]   EVIDENCE THAT THE HYPOTHALAMUS MAY BE A SOURCE OF A CIRCULATING NA+-K+-ATPASE INHIBITOR [J].
ALAGHBANDZADEH, J ;
FENTON, S ;
HANCOCK, K ;
MILLETT, J ;
DEWARDENER, HE .
JOURNAL OF ENDOCRINOLOGY, 1983, 98 (02) :221-226
[9]   ROLE OF THE NA+ PUMP IN SMOOTH-MUSCLE CONTRACTILE REGULATION [J].
ALLEN, JC ;
NAVRAN, SS .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1984, 5 (11) :462-465
[10]   NA+-K+-ATPASE IN VASCULAR SMOOTH-MUSCLE [J].
ALLEN, JC ;
NAVRAN, SS ;
KAHN, AM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 250 (04) :C536-C539