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Titolo:
Modulation of aldosterone-induced stimulation of ENaC synthesis by changing the rate of apical Na+ entry
Autore:
Dijkink, L; Hartog, A; Van Os, CH; Bindels, RJM;
Indirizzi:
Univ Med Ctr Nijmegen, Dept Cell Physiol, NL-6500 HB Nijmegen, NetherlandsUniv Med Ctr Nijmegen Nijmegen Netherlands NL-6500 HB megen, Netherlands
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 4, volume: 281, anno: 2001,
pagine: F687 - F692
SICI:
0363-6127(200110)281:4<F687:MOASOE>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPITHELIAL SODIUM-CHANNEL; CORTICAL COLLECTING TUBULE; SALIVARY DUCT CELLS; HOMOLOGOUS SUBUNITS; MEDIATED REGULATION; INTRACELLULAR NA+; RABBIT KIDNEY; ALPHA-SUBUNIT; CYTOSOLIC NA+; TRANSPORT;
Keywords:
rabbit kidney; cortical collecting duct; connecting tubule; epithelial sodium channel; benzamil;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Bindels, RJM Univ Med Ctr Nijmegen, Dept Cell Physiol, POB 9101, NL-6500 HB Nijmegen, Netherlands Univ Med Ctr Nijmegen POB 9101 Nijmegen Netherlands NL-6500 HB
Citazione:
L. Dijkink et al., "Modulation of aldosterone-induced stimulation of ENaC synthesis by changing the rate of apical Na+ entry", AM J P-REN, 281(4), 2001, pp. F687-F692

Abstract

Primary cultures of immunodissected rabbit connecting tubule and cortical collecting duct cells were used to investigate the effect of apical Na+ entry rate on aldosterone-induced transepithelial Na+ transport, which was measured as benzamil-sensitive short-circuit current (I-sc). Stimulation of the apical Na+ entry, by long-term short-circuiting of the monolayers, suppressed the aldosterone-stimulated benzamil-sensitive I-sc from 320 +/- 49 to 117 +/- 14%, whereas in the presence of benzamil this inhibitory effect wasnot observed (335 +/- 74%). Immunoprecipitation of [S-35] methionine-labeled beta -rabbit epithelial Na+ channel (rbENaC) revealed that the effects of modulation of apical Na+ entry on transepithelial Na+ transport are exactly mirrored by beta -rbENaC protein levels, because short-circuiting the monolayers decreased aldosterone-induced beta -rbENaC protein synthesis from 310 +/- 51 to 56 +/- 17%. Exposure to benzamil doubled the beta -rbENaC protein level to 281 +/- 68% in control cells but had no significant effect onaldosterone-stimulated beta -rbENaC levels (282 +/- 68%). In conclusion, stimulation of apical Na+ entry suppresses the aldosterone-induced increase in transepithelial Na+ transport. This negative-feedback inhibition is reflected in a decrease in beta -rbENaC synthesis or in an increase in beta -rbENaC degradation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 04:25:37