Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
HCO3- reabsorption in renal collecting duct of NHE-3- deficient mouse: a compensatory response
Autore:
Nakamura, S; Amlal, H; Schultheis, PJ; Galla, JH; Shull, GE; Soleimani, M;
Indirizzi:
Univnnati,nnati, Dept Internal Med, Div Nephrol & Hypertens, Sch Med, Cinci Univ Cincinnati Cincinnati OH USA 45267 phrol & Hypertens, Sch Med, Cinci Univ Cincinnati, Sch Med, Dept Mol Genet, Cincinnati, OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 l Genet, Cincinnati, OH 45267 USA UnivACincinnati, Sch Med, Dept Biochem & Microbiol, Cincinnati, OH 45267 US Univ Cincinnati Cincinnati OH USA 45267 icrobiol, Cincinnati, OH 45267 US
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 6, volume: 45, anno: 1999,
pagine: F914 - F921
SICI:
0363-6127(199906)45:6<F914:HRIRCD>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
H+-K+-ATPASE; BICARBONATE TRANSPORT; INTERCALATED CELLS; NA+/H+ EXCHANGER; PROXIMAL TUBULE; ALKALI LOADS; ACID; KIDNEY; RAT; EXPRESSION;
Keywords:
acid-base; proton-potassium-adenosinetriphosphatase; AE-1; proton-adenosinetriphosphatase; bicarbonate reabsorption; cortical collecting duct; outer medullary collecting duct; NHE-3 knockout;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Soleimani, M Univethesdanati, Dept Internal Med, Div Nephrol & Hypertens, Sch Med, 231 B Univ Cincinnati 231 Bethesda Ave,MSB 5502 Cincinnati OH USA 45267
Citazione:
S. Nakamura et al., "HCO3- reabsorption in renal collecting duct of NHE-3- deficient mouse: a compensatory response", AM J P-REN, 45(6), 1999, pp. F914-F921

Abstract

Mice with a targeted disruption of Na+/H+ exchanger NHE-3 gene show significant reduction in HCO3- reabsorption in proximal tubule, consistent with the absence of NHE-3. Serum HCO3-, however, is only mildly decreased (P. Schulties, L. L. Clarke, P. Meneton, M. L. Miller, ill. Soleimani, L. R. Gawenis, T. M. Riddle, J. J. Duffy, T Doetschman, T. Wang, G. Giebisch, P. S. Aronson, J. N. Lorenz, and G. E. Shull. Nature Genet. 19: 282-285, 1998), indicating possible adaptive upregulation of HCO(3)(-)absorbing transporters in collecting duct of NHE-3-deficient (NHE-3 -/-) mice. Cortical collecting duct (CCD) and outer medullary collecting duct (OMCD) were perfused, and total CO2 (net HCO3- flux, J(tCO2)) was measured in the presence of 10 mu M Schering 28080 (SCH, inhibitor of gastric H+-K+-ATPase) or 50 mu M diethylestilbestrol (DES, inhibitor of Hf-ATPase) in both mutant and wild-type (WT) animals. In CCD, J(tCO2) increased in NHE-3 mutant mice (3.42 +/- 0.28 in WT to 5.71 +/- 0.39 pmol min-l mm tubule-l in mutants, P < 0.001). The SCH-sensitive net HCO, flux remained unchanged, whereas the DES-sensitive HCO3- flux increased in the CCD of NHE-3 mutant animals. In OMCD, J(tCO2) increased in NHE-3 mutant mice (8.8 +/- 0.7 in WT to 14.2 +/- 0.6 pmol.min(-1).mm tubule-1 in mutants, P < 0.001). Both the SCH-sensitive and the DES-sensitive HCO3- fluxes increased in the OMCD of NHE-3 mutant animals. Northern hybridizations demonstrated enhanced expression of the basolateral Cl-/HCO3-, exchanger (AE-1) mRNA in the cortex. The gastric H+-K+-ATPase mRNA showed upregulation in the medulla but not the cortex of NHE-3 mutant mice. Our results indicate that HCO3- reabsorption is enhanced in CCD and OMCD of NHE-3-deficient mice. In CCD, H+-ATPase, and in the OMCD, both H+-ATPase and gastric H+-K+-ATPase contribute to the enhanced compensatory HCO3- reabsorptionin NHE-3-deficient animals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 08:09:40