title: The basis of higher Na+ transport by inner medullary collecting duct cells from Dahl salt-sensitive rats: implicating the apical membrane Na+ channel.
abstract: The present experiments were designed to examine the function of Na/K pumps from Dahl salt-sensitive (S) and salt-resistant (R) rats. Previous reports have suggested that there is a difference in primary sequence in the alpha 1 subunit, the major Na/K pump isoform in the kidney. This sequence difference might contribute to differences in NaCl excretion in these two strains which in turn could influence the systemic blood pressure. Using "back-door" phosphorylation of pumps isolated from basolateral membranes of kidney cortex, we found no differences between S and R strains. We also examined the Na/K pumps from cultured inner medullary collecting duct (IMCD) cells. This approach takes advantage of the fact that monolayers cultured from S rats transport about twice as much Na+ as monolayers cultured from R rats. In cells whose apical membrane was made permeable with amphotericin B, comparison of the affinities for ouabain, Na+, and K+, respectively, showed only small or no differences between S and R monolayers. Ouabain binding showed no difference in the number of Na/K pumps on the basolateral membrane of cultured cells, despite a 2-fold difference in Na+ transport rates. The analysis of the steady-state Na+ transport indicates that Na/K pumps in IMCD monolayers from S rats operate at a higher fraction of their maximum capacity than do pumps in monolayers from R rats. The results, taken together, suggest that the major reason for the higher rate of Na+ transport in S monolayers is because of a primary increase in the conductive permeability of the apical membrane to Na+. They suggest that the epithelial Na+ channel is intrinsically different or differently regulated in S and R rats.
authors.affiliation: Department of Internal Medicine, University of Iowa, Iowa City 52242, USA.
authors.forename: R F
authors.initials: RF
authors.lastname: Husted
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
authors.forename: J B
authors.initials: JB
authors.lastname: Stokes
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D004351:Drug Resistance; D004553:Electric Conductivity; D006973:Hypertension / Q000209:etiology / Q000378:metabolism; D017136:Ion Transport; D007679:Kidney Medulla / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D007700:Kinetics; D010042:Ouabain / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism*; D012982:Sodium, Dietary / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D015222:Sodium Channels; D012982:Sodium, Dietary; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase