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Titolo:
RAPID REDISTRIBUTION AND INHIBITION OF RENAL SODIUM TRANSPORTERS DURING ACUTE PRESSURE NATRIURESIS
Autore:
ZHANG YB; MIRCHEFF AK; HENSLEY CB; MAGYAR CE; WARNOCK DG; CHAMBREY R; YIP KP; MARSH DJ; HOLSTEINRATHLOU NH; MCDONOUGH AA;
Indirizzi:
UNIV SO CALIF,SCH MED,DEPT PHYSIOL & BIOPHYS,1333 SAN PABLO ST LOS ANGELES CA 90033 UNIV SO CALIF,SCH MED,DEPT PHYSIOL & BIOPHYS LOS ANGELES CA 90033 UNIV ALABAMA,DEPT MED,CTR NEPHROL RES & TRAINING,VASC BIOL & HYPERTENS PROGRAM BIRMINGHAM AL 35294 DEPT VET AFFAIRS BIRMINGHAM AL 35294 BROWN UNIV,SCH MED,DEPT PHYSIOL PROVIDENCE RI 02912 UNIV COPENHAGEN,INST EXPTL MED DK-2200 COPENHAGEN N DENMARK
Titolo Testata:
American journal of physiology. Renal, fluid and electrolyte physiology
fascicolo: 6, volume: 39, anno: 1996,
pagine: 1004 - 1014
SICI:
0363-6127(1996)39:6<1004:RRAIOR>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
NA+-K+-ATPASE; PROXIMAL CONVOLUTED TUBULE; PERFUSION-PRESSURE; CARBONIC-ANHYDRASE; BETA-SUBUNIT; RAT; MEMBRANE; CELLS; LOCALIZATION; KIDNEY;
Keywords:
MEMBRANE TRAFFICKING; SODIUM-POTASSIUM-ACTIVATED ADENOSINE-TRIPHOSPHATASE; NHE3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
Y.B. Zhang et al., "RAPID REDISTRIBUTION AND INHIBITION OF RENAL SODIUM TRANSPORTERS DURING ACUTE PRESSURE NATRIURESIS", American journal of physiology. Renal, fluid and electrolyte physiology, 39(6), 1996, pp. 1004-1014

Abstract

Acute arterial hypertension provokes a rapid decrease in proximal tubule (PT) Nai reabsorption, increasing flow to the macula densa, the signal for tubuloglomerular feedback. We tested the hypothesis, in rats,that Na+ transport is decreased due to rapid redistribution of apicalNa+/H+ exchangers and basolateral Na+ pumps to internal membranes. Arterial pressure was increased 50 mmHg by constricting various arteries. We also tested whether transporter internalization occurred when PT Na+ reabsorption was inhibited with the carbonic anhydrase inhibitor benzolamide. Five minutes after initiating either natriuretic stimuli, cortex was removed, and membranes were fractionated by density gradient centrifugation. Urine output and endogenous lithium clearance increased threefold in response to either stimuli. Acute hypertension provoked a redistribution of apical Na+/H+ exchanger NHE3, alkaline phosphatase, and dipeptidyl peptidase IV to higher density membranes enriched in the intracellular membrane markers. Basolateral membrane Na+-K+-adenosinetriphosphatase (Na+-K+-ATPase) activity decreased 50%, 25-30% ofthe alpha(1)- and beta(1)-subunits redistributed to higher density membranes, and the remainder is attributed to decreased activity of the transporters. Benzolamide did not alter Na+ transporter activity or distribution, implying that decreasing apical Na+ uptake does not initiate redistribution or inhibition of basolateral Na+-K+-ATPase. We conclude that PT natriuresis provoked by acute arterial pressure is mediated by both endocytic removal of apical Na+/H+ exchangers and basolateral Na+ pumps as well as decreased total Na+ pump activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 07:26:44