CYTOSOLIC PH REGULATION IN CHICKEN ENTEROCYTES - NA-INDEPENDENT REGULATORY CELL ALKALINIZATION()

The mechanisms involved in intracellular pH (pH(i)) recovery from an a cid load have been investigated in enterocytes isolated from chicken. Following an intracellular acidification, by abrupt withdrawal of NH4C l,pH(i) alkalinized in the nominally absence of Na+ and bicarbonate. T his Na+- and bicarbonate-independent (NBI) regulatory cell alkalinizat ion became negligible when the pH(i) has reached a value of approx. 6. 85. Addition of Na+ induced a rapid pH(i) recovery to control values. Rotenone, DCCD, vanadate, NBD-Cl, SCH 28080 and EIPA inhibited the NBI cell alkalinization, whereas bafilomycin A(1), ouabain and H-2-DIDS w ere without effect. Na+-dependent pH(i) recovery from an acid load was inhibited by EIPA and unaffected by SCH 28080 or DCCD. The rate of NB I cell alkalinization was a linear function of the electrochemical pro ton gradient. In high external K+ buffer plus valinomycin the line goe s through the origin. Gramicidin accelerated the rate of NBI cell alka linization, whereas it was slightly reduced by low external potassium. The results demonstrate that in intestinal epithelial cells exist at least two mechanisms for proton secretion: a Na+-H+ exchanger and a Na +- and bicarbonate-independent proton transport system. This latter me chanism appears to be a proton conductance pathway.