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. 1967 Jan;46(1):95–102. doi: 10.1172/JCI105515

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

Norman Bank 1,†, Hagop S Aynedjian 1
PMCID: PMC297024  PMID: 4959907

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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