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

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.

Collecting duct adaptation to potassium depletion.

Kidneys are the main effectors of the maintenance of potassium balance, under both normal and altered conditions of dietary potassium uptake. The collecting duct system plays a major role in this control of potassium homeostasis because most of the filtered potassium is reabsorbed between the glomerulus and the distal convoluted tubule: under normal physiological conditions or in response to potassium loading, collecting ducts adjust their rate of secretion of potassium into urine so as it matches the dietary daily intake, whereas in response to restriction of potassium ingestion, this secretion process is mostly curtailed, and a reabsorptive mechanism appears. In this short review, we analyzed the cellular and molecular mechanisms underlying transepithelial transport of potassium in the collecting duct and their adaptation in response to potassium depletion. A special emphasis is given on the axial and cellular heterogeneity of the collecting duct with regard to potassium transport and its adaptation. We also discuss the factors controlling duct hypertrophy and hyperplasia during potassium depletion and their possible relationship with the control of potassium conservation.