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Titolo:
Decreased abundance of major Na+ transporters in kidneys of rats with ischemia-induced acute renal failure
Autore:
Kwon, TH; Frokiaer, J; Han, JS; Knepper, MA; Nielsen, S;
Indirizzi:
Univ Aarhus, Inst Anat, Dept Cell Biol, DK-8000 Aarhus C, Denmark Univ Aarhus Aarhus Denmark C , Dept Cell Biol, DK-8000 Aarhus C, Denmark Aarhus Univ Hosp, Dept Clin Physiol, DK-8200 Aarhus, Denmark Aarhus Univ Hosp Aarhus Denmark DK-8200 Physiol, DK-8200 Aarhus, Denmark Inst Expt Clin Res, DK-8200 Aarhus N, Denmark Inst Expt Clin Res Aarhus Denmark N Clin Res, DK-8200 Aarhus N, Denmark Seoul Natl Univ Hosp, Dept Internal Med, Seoul 110744, South Korea Seoul Natl Univ Hosp Seoul South Korea 110744 Seoul 110744, South Korea NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA NHLBI Bethesda MD USA 20892 rolyte Metab Lab, NIH, Bethesda, MD 20892 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 6, volume: 278, anno: 2000,
pagine: F925 - F939
SICI:
0363-6127(200006)278:6<F925:DAOMNT>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
THICK ASCENDING LIMB; MELANOCYTE-STIMULATING HORMONE; K-CL COTRANSPORTER; PROXIMAL TUBULE; MOLECULAR-CLONING; ALTERED EXPRESSION; REPERFUSION INJURY; ATPASE; LOCALIZATION; AQUAPORINS;
Keywords:
sodium transport; sodium-hydrogen exchanger; sodium-inorganic; phosphate cotransporter; sodium-potassium-2 chloride; transporter; sodium-chloride cotransporter;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Nielsen, S Univ Aarhus, Inst Anat, Dept Cell Biol, DK-8000 Aarhus C, Denmark Univ Aarhus Aarhus Denmark C Biol, DK-8000 Aarhus C, Denmark
Citazione:
T.H. Kwon et al., "Decreased abundance of major Na+ transporters in kidneys of rats with ischemia-induced acute renal failure", AM J P-REN, 278(6), 2000, pp. F925-F939

Abstract

Ischemia-induced acute renal failure (ARF) is known to be associated with significant impairment of tubular Na reabsorption. We examined whether temporary bilateral renal ischemia (30, 40, or 60 min) and reperfusion (1-5 days) affect the abundance of several renal Na transporters and urinary Na excretion (UNaV) in rats. In rats with mild ARF (30 min), immunoblotting revealed that proximal tubule type 3 Na+/H+ exchanger (NHE-3) and type II Na-P-icotransporter (NaPi-II) were significantly decreased to 28 +/- 6 and 14 +/- 6% of sham levels, respectively, at day 1. Moreover, Na+-K+-ATPase levelswere also significantly decreased (51 +/- 11%), whereas there was no significant decrease in type 1 bumetanide-sensitive cotransporter (BSC-1) and thiazide-sensitive cotransporter (TSC) levels. Consistent with reduced Na transporter abundance, fractional urinary Na excretion (FENa) was significantly increased in mild ARF (30 min) and UNaV was unchanged, despite a marked reduction in glomerular filtration rate. Na transporter levels and renal Na handling were normalized within 5 days. Severe ischemic injury (60 min) resulted in a marked decrease in the abundance of Na+-K+-ATPase, NHE-3, NaPi-II, BSC-1, and TSC at both days 1 and 5. Consistent with this, FENa was significantly increased at days 1 and 5. Intravenous K-melanocyte-stimulated hormone treatment partially prevented the ischemia-induced downregulation of renal Na transporters and reduced the high FENa to control levels. We conclude that reduced levels of Na transporters along the nephron may play a critical role in the impairment of tubular Na reabsorption, and hence increased Na excretion, in ischemia-induced ARF.

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Documento generato il 05/04/20 alle ore 10:43:49