Mechanisms of the inhibition of epithelial Na+ channels by CFTR and purinergic stimulation

被引：47

作者：

Kunzelmann, K ^{[1
]}

Schreiber, R ^{[1
]}

Boucherot, A ^{[1
]}

机构：

[1] Univ Queensland, Dept Physiol & Pharmacol, Brisbane, Qld 4072, Australia

来源：

KIDNEY INTERNATIONAL | 2001年 / 60卷 / 02期

关键词：

ENaC; cystic fibrosis; UTP; ATP; purinergic stimulation; transport proteins;

D O I：

10.1046/j.1523-1755.2001.060002455.x

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

The epithelial Na+ channel ENaC is inhibited when the cystic fibrosis transmembrane conductance regulator (CFTR) coexpressed in the same cell is activated by the cyclic adenosine monophosphate (cAMP)-dependent pathway. Regulation of ENaC by CFTR has been studied in detail in epithelial tissues from intestine and trachea and is also detected in renal cells. In the kidney, regulation of other membrane conductances might be the predominant function of CFTR. A similar inhibition of ENaC takes place when luminal purinergic receptors a re activated by 5 ' -adenosine triphosphate (ATP) or uridine triphosphate (UTP). Because both stimulation of purinergic receptors and activation of CFTR induce a Cl- conductance, it is likely that Cl- ions control ENaC activity.

引用

收藏

页码：455 / 461

页数：7

相关论文

共 32 条

[1] Axial distribution and characterization of basolateral P2Y receptors along the rat renal tubule [J].

Bailey, MA ;

Imbert-Teboul, M ;

Turner, C ;

Marsy, S ;

Srai, K ;

Burnstock, G ;

Unwin, RJ .

KIDNEY INTERNATIONAL, 2000, 58 (05) :1893-1901

[2]

Bates CM, 1997, J AM SOC NEPHROL, V8, P352

[3] Extracellular ATP increases [CA2+]i in distal tubule cells.: I.: Evidence for a P2Y2 purinoceptor [J].

Bidet, M ;

De Renzis, G ;

Martial, S ;

Rubera, I ;

Tauc, M ;

Poujeol, P .

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2000, 279 (01) :F92-F101

[4] 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

[5] Cl- transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial Na+ channels (ENaCs) in Xenopus oocytes co-expressing CFTR and ENaC [J].

Briel, M ;

Greger, R ;

Kunzelmann, K .

JOURNAL OF PHYSIOLOGY-LONDON, 1998, 508 (03) :825-836

[6] IMMUNOCYTOCHEMICAL LOCALIZATION OF THE CYSTIC-FIBROSIS GENE-PRODUCT CFTR [J].

CRAWFORD, I ;

MALONEY, PC ;

ZEITLIN, PL ;

GUGGINO, WB ;

HYDE, SC ;

TURLEY, H ;

GATTER, KC ;

HARRIS, A ;

HIGGINS, CF .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (20) :9262-9266

[7] ATP stimulates Cl- secretion and reduces amiloride-sensitive Na+ absorption in M-1 mouse cortical collecting duct cells [J].

Cuffe, JE ;

Bielfeld-Ackermann, A ;

Thomas, J ;

Leipziger, J ;

Korbmacher, C .

JOURNAL OF PHYSIOLOGY-LONDON, 2000, 524 (01) :77-90

[8]

Deetjen P, 2000, J AM SOC NEPHROL, V11, P1798, DOI 10.1681/ASN.V11101798

[9] UTP inhibits Na+ absorption in wild-type and ΔF508 CFTR-expressing human bronchial epithelia [J].

Devor, DC ;

Pilewski, JM .

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1999, 276 (04) :C827-C837

[10]

DONCKERWOLCKE RA, 1992, CHILD NEPHROL UROL, V12, P186

← 1 2 3 4 →