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Am J Physiol Renal Physiol 267: F639-F645, 1994;
0363-6127/94 $5.00
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AJP - Renal Physiology, Vol 267, Issue 4 639-F645, Copyright © 1994 by American Physiological Society


ARTICLES

Physiological and immunocytochemical evidence for a putative H-K-ATPase in elasmobranch renal acid secretion

E. R. Swenson, A. D. Fine, T. H. Maren, E. Reale, E. R. Lacy and A. J. Smolka
Department of Medicine, Veterans Affairs Medical Center, Seattle, Washington.

The mechanism of renal acid secretion in marine fish is largely unknown. We explored whether H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) is present and functional in acid secretion in the kidney of the elasmobranch spiny dogfish shark, Squalus acanthias. In whole animal studies, a specific inhibitor of mammalian H(+)-K(+)-ATPase, Sch-28080, abolished greater than 87% of basal (62 mg/kg) and 75% of imidazole-stimulated titratable acid excretion (5 and 62 mg/kg). Antibodies directed against the COOH-terminus hog gastric H(+)-K(+)-ATPase alpha-subunit stained specific subdivisions of the neck, early and late proximal tubule, late intermediate tubule, both segments of the distal tubule, and the early collecting duct of the renal tubule of these fish. These findings are consistent with a major role for a protein similar to the mammalian gastric H(+)-K(+)-ATPase in elasmobranch renal acid secretion.


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