Effect of acute increases in filtered HCO3- on renal hydrogen transporters: II. H(+)-ATPase.
Adaptive increases in renal bicarbonate reabsorption occur in response to acute increases in filtered bicarbonate (FLHCO3). In a previous study, we showed that an increase in FLHCO3 induced by plasma volume expansion increased the Vmax for Na+/H+ exchange activity in renal cortical brush border membrane vesicles (BBMV), providing a potential mechanism for the adaptive increase in HCO3- reabsorption. The present studies were undertaken to determine whether the increase in FLHCO3 induced by plasma expansion also stimulates the other major H+ transporter in cortical BBMV, the H(+)-ATPase. H(+)-ATPase activity was assessed in BBMV obtained from hydropenic and plasma expanded Munich-Wistar rats, using a NADH-linked ATPase assay. H(+)-ATPase activity was measured as the ouabain and oligomycin-insensitive, bafilomycin A1-sensitive component of total ATPase activity. Acute plasma expansion doubled single nephron FLHCO3, and this change was associated with a 64% increase in the Vmax for H(+)-ATPase activity, with no change in apparent Km. The Vmax for H(+)-ATPase activity correlated directly with whole kidney GFR and FLHCO3 (r = 0.68 and 0.72, respectively), and with single nephron GFR and FLHCO3 (r = 0.76 and 0.80, respectively). Thus, the mechanism for the adaptive increase in proximal tubular HCO3- reabsorption that occurs in response to acute increases in FLHCO3 appears to be related to increased activity of both H(+)-ATPase and Na+/H+ exchange in the apical membrane of the proximal tubule epithelium.
Maddox
D A
DA
Department of Medicine, University of Vermont, College of Medicine, Burlington, USA. dmaddox@sunflowr.usd.edu
Barnes
W D
WD
Gennari
F J
FJ
D000042:Absorption; D000222:Adaptation, Physiological / Q000502:physiology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001639:Bicarbonates / Q000378:metabolism*; D001835:Body Weight; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007552:Isotonic Solutions / Q000494:pharmacology; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000201:enzymology*; D007700:Kinetics; D018942:Macrolides; D008297:Male; D008871:Microvilli / Q000378:metabolism; D009840:Oligomycins / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D010952:Plasma Substitutes / Q000494:pharmacology; D006180:Proton-Translocating ATPases / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D000077325:Ringer's Lactate; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D014462:Ultrafiltration
D000900:Anti-Bacterial Agents; D001639:Bicarbonates; D004791:Enzyme Inhibitors; D007552:Isotonic Solutions; D018942:Macrolides; D009840:Oligomycins; D010952:Plasma Substitutes; D000077325:Ringer's Lactate; D017923:Sodium-Hydrogen Exchangers; C048335:oligomycin B; D010042:Ouabain; C040929:bafilomycin A1; D000255:Adenosine Triphosphate; D006180:Proton-Translocating ATPases