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Am J Physiol Renal Physiol 279: F1053-F1059, 2000;
0363-6127/00 $5.00
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Vol. 279, Issue 6, F1053-F1059, December 2000

Cellular origin and hormonal regulation of K+-ATPase activities sensitive to Sch-28080 in rat collecting duct

Nicolas Laroche-Joubert, Sophie Marsy, and Alain Doucet

Laboratoire de Biologie Intégrée des Cellules Rénales, Service de Biologie Cellulaire, Commissariat à l'Énergie Atomique, Saclay, Unité de Recherche Associée 1859, Centre National de la Recherche Scientifique, 91191 Gif-sur-Yvette Cedex, France

Rat collecting ducts exhibit type I or type III K+-ATPase activities when animals are fed a normal (NK) or a K+-depleted diet (LK). This study aimed at determining functionally the cell origin of these two K+-ATPases. For this purpose, we searched for an effect on K+-ATPases of hormones that trigger cAMP production in a cell-specific fashion. The effects of 1-deamino-8-D-arginine vasopressin (dD-AVP), calcitonin, and isoproterenol in principal cells, alpha -intercalated cells, and beta -intercalated cells of cortical collecting duct (CCD), respectively, and of dD-AVP and glucagon in principal and alpha -intercalated cells of outer medullary collecting duct (OMCD), respectively, were examined. In CCDs, K+-ATPase was stimulated by calcitonin and isoproterenol in NK rats (type I K+-ATPase) and by dD-AVP in LK rats (type III K+-ATPase). In OMCDs, dD-AVP and glucagon stimulated type III but not type I K+-ATPase. These hormone effects were mimicked by the cAMP-permeant analog dibutyryl-cAMP. In conclusion, in NK rats, cAMP stimulates type I K+-ATPase activity in alpha - and beta -intercalated CCD cells, whereas in LK rats it stimulates type III K+-ATPase in principal cells of both CCD and OMCD and in OMCD intercalated cells.

colonic and gastric hydrogen-potassium-adenenosine triphosphatase; adenosine 3',5'-cyclic monophosphate; potassium depletion; vasopressin; glucagon; isoproterenol; calcitonin


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