title: Bicarbonate reabsorption and electrophysiology of proximal tubules in uninephrectomized rats.
abstract: 1. The kinetics of acidification of luminal fluid in hypertrophied proximal tubules after unilateral nephrectomy was studied by stationary microperfusion and continuous measurement of luminal pH with antimony microelectrodes. 2. Trans-epithelial and basolateral membrane electrical potential differences were measured in order to detect modifications in electrogenic transport mechanisms under these conditions. 3. The values of stationary pH and HCO3- concentration were significantly lower, the mean acidification half-time was not different and net reabsorptive HCO3- fluxes in proximal tubules were significantly increased in uninephrectomized rats. According to an electrical analogue model, these results suggest (a) a reduction in the internal series resistance of the H+ pump, caused perhaps by an increased density of pump sites, and (b) an increase in the protonmotive force of the pump. 4. The trans-epithelial electrical potential difference measured in free flow conditions was significantly more lumen-positive in uninephrectomized rats. The trans-epithelial electrical potential difference measured during intraluminal perfusion with Ringer solution containing 30 mmol/l HCO3- was significantly more negative in all groups studied. In uninephrectomized rats treated with acetazolamide, the trans-epithelial electrical potential difference was more lumen-negative than that in untreated uninephrectomized rats. These results are compatible with a steeper transepithelial Cl- gradient as well as with electrogenic, active H+ secretion. 5. There was no significant difference in the basolateral electrical potential difference between control and uninephrectomized rats. 6. In conclusion, our data show an increase in the transport rates of HCO3- in the proximal tubule of uninephrectomized rats, which may be due to an increase in the density of transporters in the brush-border membrane, and an increased ability of the transport mechanism to create H+ gradients.
authors.affiliation: Department of Clinical Medicine, University of Sao Paulo Medical School, Brazil.
authors.forename: D M
authors.initials: DM
authors.lastname: Limongi
authors.forename: A C
authors.initials: AC
authors.lastname: Cassola
authors.forename: V
authors.initials: V
authors.lastname: Woronik
authors.forename: G
authors.initials: G
authors.lastname: Malnic
mesh_terms: D000042:Absorption; D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001693:Biological Transport, Active; D004594:Electrophysiology; D006863:Hydrogen-Ion Concentration; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009392:Nephrectomy; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D001639:Bicarbonates; D000086:Acetazolamide