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Articles in PresS, published online ahead of print November 20, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00188.2001
Submitted on June 20, 2001
Accepted on November 16, 2001
1 Universite Pierre et Marie Curie, Institut National de la Sante et de la Recherche Medicale, Unite 356; Institut Federatif de Recherche 58, Paris, France; Hopital Europeen Georges Pompidou; Assistance Publique-Hopitaux de Paris, Paris, France
2 Universite Pierre et Marie Curie, Institut National de la Sante et de la Recherche Medicale, Unite 356; Institut Federatif de Recherche 58, Paris, France
* To whom correspondence should be addressed. E-mail: chambrey{at}ccr.jussieu.fr.
In the proximal tubule, the apical Na+/H+ exchanger identified as NHE3 mediates most of NaCl and NaHCO3 absorption. In chronic metabolic acidosis, enhanced proximal tubule bicarbonate absorption is associated with an increase in NHE3 protein abundance and activity. In contrast, the response of proximal tubule to chronic metabolic alkalosis remains controversial. The kidney responds to chronic changes in NaCl intake by modifying urinary sodium excretion, but it is not clear whether alterations in proximal tubule Na+ transport contribute to this adaptation. The purpose of these studies was to analyze the long-term regulation of the proximal Na+/H+ exchanger NHE3 during alkalosis induced by dietary NaHCO3 loading and changes in NaCl intake. Sprague Dawley rats exposed to a low NaCl, high NaCl or NaHCO3 diet for 6 days were studied. Control groups had access to regular food and tap water. Rats were kept in metabolic cages to determine daily urinary electrolyte excretion. At the end of the experiment, serum electrolyte levels and renin activity were measured. Renal cortical apical membrane vesicles (AMV) were prepared from treated and normal rats. Na+/H+ exchange was assayed as the initial rate of 22Na+ uptake in the presence of an outward H+ gradient. 22Na+ uptake measured in the presence of high dose EIPA were not different in any model. Addition of 30 µM HOE 642 had no significant effect on 22Na+ uptake in any model, indicating that NHE3 alone contributed to proximal apical Na+ /H+ exchange. Changes in NaCl intake did not affect NHE3 activity whereas NaHCO3 loading inhibited 22Na+ uptake by 30%. AMV NHE3 protein abundance assessed by Western blot was unaffected during changes of NaCl intake. During NaHCO3 loading, NHE3 protein abundance was decreased by 65% whereas the expression level of an other brush-border membrane protein, the Na-glucose cotransporter type 1, remained unchanged. We conclude that renal adaptation to chronic modifications in sodium intake does not include changes in proximal NHE3 expression level and activity whereas NHE3 appears appropriately regulated during chronic metabolic acid-base disorders.
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