Mechanism Of HCO3 Research Articles

HCO3- transport in basolateral membrane vesicles isolated from rat renal cortex.

The mechanism of HCO3- translocation across the proximal tubule basolateral membrane was investigated by testing for Na+-HCO3- cotransport using isolated membrane vesicles purified from rat renal cortex. As indicated by 22Na+ uptake, imposing an inwardly directed HCO3- concentration gradient induced the transient concentrative accumulation of intravesicular Na+. The stimulation of basolateral membrane vesicle Na+ uptake was specifically HCO3(-)-dependent as only basolateral membrane-independent Na+ uptake was stimulated by an imposed hydroxyl gradient in the absence of HCO3-. No evidence for Na+-HCO3- cotransport was detected in brush border membrane vesicles. Charging the vesicle interior positive stimulated net intravesicular Na+ accumulation in the absence of other driving forces via a HCO3(-)-dependent pathway indicating the flow of negative charge accompanies the Na+-HCO3- cotransport event. Among the anion transport inhibitors tested, 4-4'-diisothiocyanostilbene-2,2'-disulfonic acid demonstrated the strongest inhibitor potency at 1 mM. The Na+-coupled transport inhibitor harmaline also markedly inhibited HCO3- gradient-driven Na+ influx. A role for carbonic anhydrase in the mechanism of Na+-HCO3- cotransport is suggested by the modest inhibition of HCO3- gradient driven Na+ influx caused by acetazolamide. The imposition of Cl- concentration gradients had a marked effect on HCO3- gradient-driven Na+ influx which was furosemide-sensitive and consistent with the operation of a Na+-HCO3- for Cl- exchange mechanism. The results of this study provide evidence for an electrogenic Na+-HCO3- cotransporter in basolateral but not microvillar membrane vesicles isolated from rat kidney cortex. The possible existence of an additional basolateral membrane HCO3(-)-translocating pathway mediating Na+-HCO3- for Cl- exchange is suggested.

HCO3 transport in rat jejunum: relationship to NaCl and H2O transport in vivo.

HCO3- absorption and its association with Na+ absorption has been studied in the rat jejunum in vivo, using a single-pass perfusion technique. The method of disequilibrium pH, the only valid way of demonstrating jejunal H+ secretion, was used to distinguish between an HCO3- pump and H+ secretion as the mechanism of HCO3- absorption. HCO3- stimulated Na+ absorption; Na+ deletion inhibited HCO3 absorption, decreased luminal acidification, and decreased the level of luminal PCO2. These results confirmed an Na+:H+ cation exchange, the possible mechanism of which is discussed in terms of results using other tissues. Na+-dependent HCO3-absorption made up a larger part of total HCO3-absorption as the luminal HCO3-concentrations diminished, although the precise degree of Na+-dependency could not be determined because of the unstirred layer effect. The mechanism of Na+-independent HCO3-absorption was not established, but it was not affected by PD, Cl-, or H2O movements. Glucose-stimulated and HCO3-stimulated Na+ absorption were less than additive. The physiological importance of HCO3-stimulated Na+ absorption in the acidic postprandial jejunum is probably due entirely to the effect of free CO2 in the lumen.