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1 Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut 06269; 2 Department of Pharmacology and Therapeutics, University of Florida Health Science Center, Gainesville, Florida 32610; 3 Department of Veterans Affairs Medical Center and University of Washington, Seattle, Washington 98108; and 4 Mount Desert Island Biological Laboratory, Salsbury Cove, Maine 04672
Though chemical
assays indicate that carbonic anhydrase (CA) activity is present in
marine teleost nephrons, CA inhibitors have no effect on urine pH or
bicarbonate excretion, parameters typically CA dependent in almost all
vertebrate groups. Because marine teleost renal sulfate secretion is
associated with bicarbonate anion exchange, we investigated the effect
of CA inhibition on transepithelial sulfate transport by flounder renal
tubule primary monolayer cultures (PTC) and on renal sulfate secretion
(
SO4) by intact flounder. Both methazolamide and ethoxzolamide (10 µM) inhibited PTC secretory flux by ~50%; reabsorptive sulfate flux, Na-dependent glucose transport, and transepithelial electrical resistance were unaffected. A CA inhibitor restricted to the
extracellular space (10 µM polyoxyethylene-aminobenzolamide,
3.7 kDa) had no effect on PTC sulfate transport. Intravenous
administration of methazolamide reduced
SO4
almost 40% and had no effect on glomerular filtration rate (GFR),
urine flow rate, or Pi excretion
rate. Serum pH was significantly reduced 0.2 units, whereas urine pH was unchanged. Together, the in vitro and in vivo results indicate that
CA facilitates renal sulfate secretion in the seawater teleost.
anion exchange; sulfate clearance; methazolamide; ethoxzolamide; winter flounder; fish renal function; acid-base balance
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