A Microperfusion Study of Bicarbonate Accumulation in the Proximal Tubule of the Rat Kidney

Norman Bank; Hagop S. Aynedjian

doi:10.1172/JCI105515

A Microperfusion Study of Bicarbonate Accumulation in the Proximal Tubule of the Rat Kidney

Norman Bank and Hagop S. Aynedjian

Published January 1, 1967 - More info

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Abstract

In order to determine whether HCO₃^- gains access to the proximal tubular lumen from a source other than the glomerular filtrate, we carried out microperfusion experiments on isolated segments of rat proximal tubules in vivo. The perfusion fluid was essentially free of HCO₃^- and of a composition that prevented net absorption of sodium and water.

It was found that when plasma HCO₃^- concentration and CO₂ tension (PCO₂) were normal, the HCO₃^- concentration in the collected perfusate rose to about 3 mEq per L. Inhibition of renal carbonic anhydrase did not produce an appreciable change in this value in normal rats, but when the enzyme was inhibited in acutely alkalotic rats, a mean concentration of 15 mEq per L was recovered in the perfusate. Addition of HCO₃^- to the tubular lumen might occur by either intraluminal generation of HCO₃^- from CO₂ and OH^- or by influx of ionic bicarbonate from the plasma or tubular cells. Because of the marked increase in HCO₃^- found when intraluminal carbonic anhydrase was inhibited, generation of new HCO₃^- from CO₂ and OH^- seems unlikely. We conclude, therefore, that influx of ionic bicarbonate occurred, either across the luminal membrane or through extracellular aqueous channels. These observations suggest that the proximal epithelium has a finite degree of permeability to HCO₃^- and that influx of this ion may be a component of the over-all handling of HCO₃^- by the kidney.