Secretion of bicarbonate has been described for distar nephron epithel
ium and attributed to apical Cl-/HCO3- exchange in beta-intercalated c
ells. We investigated the presence of this mechanism in cortical dista
l tubules by perfusing these segments with acid (pH 6) 10 mM phosphate
Ringer. The kinetics of luminal alkalinization was studied in station
ary microperfusion experiments by double-barreled pH (ion-exchange res
in)/1 M KCI reference microelectrodes. Luminal alkalinization may be d
ue to influx (into the lumen) of HCO3- or OH-, or efflux of H+. The ma
gnitude of the Cl-/HCO(3)(-)xchange component was measured by perfusin
g the lumen with solutions with or without chloride, which was substit
uted by gluconate. This component was not different from zero in contr
ol and alkalotic (chronic plus acute) Wistar rats. Homozygous Brattleb
oro rats (BRB), genetically devoid of antidiuretic hormone, were used
since this hormone has been shown to stimulate H+ secretion, which cou
ld mask bicarbonate secretion. In these rats, no evidence for Cl-/HCO3
- exchange was found in control BRB and in early distal segments of al
kalotic animals, but in late distal tubule a significant component of
0.14 +/- 0.033 nmol/cm(2) sec was observed, which, however, is small w
hen compared to the reabsorptive flow found in control Wistar rats, of
0.95 +/- 0.10 nmol/cm(2) sec. In addition, 5 x 10(-4) M SITS had no e
ffect on distal bicarbonate reabsorption in controls as well as on sec
retion in alkalotic Wistar and Brattleboro rats, which is compatible w
ith the absence of effect of this drug on the apical Cl- /HCO3- exchan
ge in other tissues. It is concluded that most distal allcalinization
is not Cl- dependent, and that Cl-/HCO3- exchange may be found in cort
ical distal tubule, but its magnitude is, even in alkalosis, markedly
smaller than the reabsorptive flux, which predominates in the rats stu
died in this paper, keeping luminal pH lower than that of blood.