The absence of renal bicarbonate reabsorption maxima during carbonic anhydrase inhibition.
Present studies were performed to examine the effect of carbonic anhydrase inhibition on bicarbonate reabsorption under experimental conditions where extracellular fluid volume expansion was minimized. The data showed no tubular maximum for bicarbonate reabsorption in the normal state or after carbonic anhydrase inhibition. The data support a model which assumes that the bicarbonate reabsorption is accomplished by two processes. One process is independent of protonation from H+ secretion into the tubule and probably involves reabsorption of bicarbonate ion as such. This process has an unlimited capacity for reabsorption of bicarbonate. The contribution of this process increases with an increase in plasma bicarbonate. The second process is dependent on protonation, through the intracellular hydration of carbon dioxide. The relative contribution, through the intracellular hydration of carbon dioxide. The relative contribution of this process is normally about 33% and decreases with increased plasma bicarbonate.
D000042:Absorption; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002245:Carbon Dioxide / Q000097:blood / Q000652:urine; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology*; D002256:Carbonic Anhydrases / Q000502:physiology; D003404:Creatinine / Q000097:blood / Q000378:metabolism / Q000652:urine; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005110:Extracellular Space / Q000187:drug effects; D005919:Glomerular Filtration Rate; D006863:Hydrogen-Ion Concentration; D007263:Infusions, Parenteral; D007668:Kidney / Q000378:metabolism*; D008297:Male
D001639:Bicarbonates; D002257:Carbonic Anhydrase Inhibitors; D002245:Carbon Dioxide; D003404:Creatinine; D002256:Carbonic Anhydrases