Physiological and pathophysiological role of the epithelial sodium channel in the control of blood pressure

被引:14
作者
Hummler, E
Rossier, BC
机构
[1] Instilut de Pharmacologie et de Toxicologic de I’Université, Lausanne
关键词
sodium reabsorption; hypertension; hypotension; transgenic mice; human disease; mouse model; kidney; pseudoaldosteronism;
D O I
10.1159/000174065
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Blood pressure regulation is an integrated physiological phenomenon known to be influenced by many biological processes and by a variety of environmental factors. Epidemiological studies nevertheless suggest that up to 30% of the variation in blood pressure could be due to genetic factors. Thus, mutations in genes that control blood pressure may be the underlying cause of essential hypertension. Arterial blood pressure is critically dependent on the sodium balance and the regulation of renal sodium excretion is one of the most important homeostatic functions of the body. The identification of genes encoding proteins that transport Na+ across cells of the kidney tubules and of those regulating the activity of these sodium-transporting proteins will therefore bring further insights into the pathophysiology of salt-sensitive hypertension.
引用
收藏
页码:160 / 165
页数:6
相关论文
共 49 条
[1]   LIDDLES SYNDROME REVISITED - A DISORDER OF SODIUM-REABSORPTION IN THE DISTAL TUBULE [J].
BOTEROVELEZ, M ;
CURTIS, JJ ;
WARNOCK, DG .
NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (03) :178-181
[2]   EVIDENCE FOR REDUCED CL- AND INCREASED NA+ PERMEABILITY IN CYSTIC-FIBROSIS HUMAN PRIMARY-CELL CULTURES [J].
BOUCHER, RC ;
COTTON, CU ;
GATZY, JT ;
KNOWLES, MR ;
YANKASKAS, JR .
JOURNAL OF PHYSIOLOGY-LONDON, 1988, 405 :77-103
[3]   AMILORIDE-SENSITIVE EPITHELIAL NA+ CHANNEL IS MADE OF 3 HOMOLOGOUS SUBUNITS [J].
CANESSA, CM ;
SCHILD, L ;
BUELL, G ;
THORENS, B ;
GAUTSCHI, I ;
HORISBERGER, JD ;
ROSSIER, BC .
NATURE, 1994, 367 (6462) :463-467
[4]   EPITHELIAL SODIUM-CHANNEL RELATED TO PROTEINS INVOLVED IN NEURODEGENERATION [J].
CANESSA, CM ;
HORISBERGER, JD ;
ROSSIER, BC .
NATURE, 1993, 361 (6411) :467-470
[5]   Renal abnormalities in mutant mice [J].
Carpenter, C ;
Honkanen, AA ;
Mashimo, H ;
Goss, KA ;
Huang, P ;
Fishman, MC ;
Asaad, M ;
Dorso, CR ;
Cheung, HS .
NATURE, 1996, 380 (6572) :292-292
[6]   Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1 [J].
Chang, SS ;
Grunder, S ;
Hanukoglu, A ;
Rosler, A ;
Mathew, PM ;
Hanukoglu, I ;
Schild, L ;
Lu, Y ;
Shimkets, RA ;
NelsonWilliams, C ;
Rossier, BC ;
Lifton, RP .
NATURE GENETICS, 1996, 12 (03) :248-253
[7]   A SALT WASTING SYNDROME IN INFANCY [J].
CHEEK, DB ;
PERRY, JW .
ARCHIVES OF DISEASE IN CHILDHOOD, 1958, 33 (169) :252-256
[8]   THE WW DOMAIN OF YES-ASSOCIATED PROTEIN BINDS A PROLINE-RICH LIGAND THAT DIFFERS FROM THE CONSENSUS ESTABLISHED FOR SRC HOMOLOGY 3-BINDING MODULES [J].
CHEN, HI ;
SUDOL, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (17) :7819-7823
[9]   PSEUDOHYPOALDOSTERONISM [J].
DILLON, MJ ;
LEONARD, JV ;
BUCKLER, JM ;
OGILVIE, D ;
LILLYSTONE, D ;
HONOUR, JW ;
SHACKLETON, CHL .
ARCHIVES OF DISEASE IN CHILDHOOD, 1980, 55 (06) :427-434
[10]   DEVELOPMENTAL AND ABNORMAL-CELL DEATH IN C-ELEGANS [J].
DRISCOLL, M ;
CHALFIE, M .
TRENDS IN NEUROSCIENCES, 1992, 15 (01) :15-19