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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/F208    most recent 00468.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Pelis, R. M. Articles by Renfro, J. L. Search for Related Content PubMed PubMed Citation Articles by Pelis, R. M. Articles by Renfro, J. L.

Stimulation of renal sulfate secretion by metabolic acidosis requires Na⁺/H⁺ exchange induction and carbonic anhydrase

¹Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut; ²Department of Physiology and Pharmacology, James Cook University, Cairns, Australia; ³Department of Biology, University of Virginia's College at Wise, Wise, Virginia; ⁴Department of Biology, Georgia Southern University, Statesboro, Georgia; and ⁵Mount Desert Island Biological Laboratory, Salisbury Cove, Maine

Submitted 27 December 2004 ; accepted in final form 24 February 2005

The acute effect of metabolic acidosis on SO₄^2– secretion by the marine teleost renal proximal tubule was examined. Metabolic acidosis was mimicked in primary cultures of winter flounder renal proximal tubule epithelium (fPTCs) mounted in Ussing chambers by reducing interstitial pH to 7.1 (normally 7.7). fPTCs with metabolic acidosis secreted SO₄^2– at a net rate that was 40% higher than in paired isohydric controls (pH 7.7 on interstitium). The stimulation was completely blocked by the carbonic anhydrase inhibitor methazolamide (100 µM). Although Na⁺/H⁺ exchange (NHE) isoforms 1, 2, and 3 were identified in fPTCs by immunoblotting, administering EIPA (20 µM) to the interstitial and luminal bath solutions had no effect on net SO₄^2– secretion by fPTCs with a normal interstitial pH of 7.7. However, EIPA (20 µM) blocked most of the stimulation caused by acidosis when applied to the lumen but not interstitium, demonstrating that induction of brush-border NHE activity is important. In the intact flounder, serum pH dropped 0.4 pH units (pH 7.7 to 7.3, at 2–3 h) when environmental pH was lowered from 7.8 to 4.3. Whereas serum [SO₄^2–] was not altered by acidosis, renal tubular SO₄^2– secretion rate was elevated 200%. Thus metabolic acidosis strongly stimulates renal sulfate excretion most likely by a direct effect on active renal proximal tubule SO₄^2– secretion. This stimulation appears to be dependent on inducible brush-border NHE activity.

proximal tubule; epithelial transport; metabolic alkalosis; transport metabolon; marine teleost