MECHANISM OF APICAL AND BASOLATERAL NA-INDEPENDENT CL- BASE-EXCHANGE IN THE RABBIT SUPERFICIAL PROXIMAL STRAIGHT TUBULE()

The present study was undertaken to determine the magnitude and mechan ism of base transport via the apical and basolateral Na+-independent C l-/base exchangers in rabbit isolated perfused superficial S-2 proxima l tubules. The results demonstrate that there is an apical Na+-indepen dent Cl-/ base exchanger on both membranes. HCO3- fails to stimulate a pical Cl-/base exchange in contrast to the basolateral exchanger. Inhi bition of endogenous HCO3- production does not alter the rate of apica l Cl-/base exchange in Hepes-buffered solutions. Both exchangers are i nhibited by H2DIDS and furosemide; however, the basolateral anion exch anger is more sensitive to these inhibitors. The results indicate that the apical and basolateral Cl-/base exchangers differ in their transp ort properties and are able to transport base equivalents in the absen ce of formate. The formate concentration in rabbit arterial serum is s imilar to 6 mu M and in vitro tubule formate production is < 0.6 pmol/ min per mm. Formate in the micromolar range stimulates J(v) in a dose- dependent manner in the absence of a transepithelial Na+ and Cl- gradi ent and without a measurable effect on Cl--induced equivalent base flu x. Apical formic acid recycling cannot be an important component of an y cell model, which accounts for formic acid stimulation of transcellu lar NaCl transport in the rabbit superficial S-2 proximal tubule. We p ropose that transcellular NaCl transport in this nephron segment is me diated by an apical Na+/H+ exchanger in parallel with a Cl-/OH- exchan ger and that the secreted H+ and OH- ions form H2O in the tubule lumen .