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Titolo:
Renal salt wasting in mice lacking NHE3 Na+/H+ exchanger but not in mice lacking NHE2
Autore:
Ledoussal, C; Lorenz, JN; Nieman, ML; Soleimani, M; Schultheis, PJ; Shull, GE;
Indirizzi:
Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati,OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 icrobiol, Cincinnati,OH 45267 USA Univ Cincinnati, Coll Med, Dept Mol & Cellular Physiol, Cincinnati, OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 Physiol, Cincinnati, OH 45267 USA Univ Cincinnati, Coll Med, Dept Internal Med, Cincinnati, OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 nal Med, Cincinnati, OH 45267 USA No Kentucky Univ, Dept Biol Sci, Highland Hts, KY 41099 USA No Kentucky Univ Highland Hts KY USA 41099 ci, Highland Hts, KY 41099 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 4, volume: 281, anno: 2001,
pagine: F718 - F727
SICI:
0363-6127(200110)281:4<F718:RSWIML>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPITHELIAL SODIUM-CHANNEL; THICK ASCENDING LIMB; RAT NA/H EXCHANGER; PSEUDOHYPOALDOSTERONISM TYPE-1; BARTTERS-SYNDROME; HYPOKALEMIC ALKALOSIS; CHLORIDE TRANSPORT; CONVOLUTED TUBULE; CL COTRANSPORTER; APICAL MEMBRANE;
Keywords:
sodium absorption; sodium/hydrogen exchanger; slc9a2; slc9a3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Shull, GE Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, 231 Albert Sabin Way,ML 524, Cincinnati, OH 45267 USA Univ Cincinnati 231 Albert Sabin Way,ML 524 Cincinnati OH USA 45267
Citazione:
C. Ledoussal et al., "Renal salt wasting in mice lacking NHE3 Na+/H+ exchanger but not in mice lacking NHE2", AM J P-REN, 281(4), 2001, pp. F718-F727

Abstract

To study the role of Na+/H+ exchanger isoform 2 (NHE2) and isoform 3 (NHE3) in sodium-fluid volume homeostasis and renal Na+ conservation, mice with Nhe2 (Nhe2(-/-)) and/or Nhe3 (Nhe3(-/-)) null mutations were fed a Na+-restrieted diet, and urinary Na excretion, blood pressure, systemic acid-base and electrolyte status, and renal function were analyzed. Na+-restricted Nhe2(-/-) mice, on either a wild-type or Nhe3 heterozygous mutant (Nhe3(+/-)) background, did not exhibit excess urinary Na+ excretion. After 15 days of Na+ restriction, blood pressure, fractional excretion of Na+, and the glomerular filtration rate (GFR) of Nhe2(-/-)Nhe3(+/-) mice were similar to those of Nhe2(+/+) and Nhe3(+/-) mice, and no metabolic disturbances were observed. Nhe3(-/-) mice maintained on a Na+-restricted diet for 3 days exhibited hyperkalemia, urinary salt wasting, acidosis, sharply reduced blood pressure and GFR, and evidence of hypovolemic shock. These results negate the hypothesis that NHE2 plays an important renal function in sodium-fluid volumehomeostasis; however, they demonstrate that NHE3 is critical for systemic electrolyte, acid-base, and fluid volume homeostasis during dietary Na+ restriction and that its absence leads to renal salt wasting.

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Documento generato il 02/04/20 alle ore 19:05:27