Developmental changes in rabbit juxtamedullary proximal convoluted tubule acidification.

The transporters responsible for apical proton secretion were examined in neonatal and adult proximal convoluted tubules (PCT). Transporter activity was assayed from the rate of recovery of cell pH after cell acidification following exposure to NH4Cl. Cell pH was monitored in in vitro perfused tubules using the pH sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. Recovery from an acid load in adult PCT occurred at 0.52 +/- 0.09 pH units/min in the presence of sodium and 0.25 +/- 0.05 in the absence of sodium (p less than 0.05). One mmol/L N-ethylmaleimide, an inhibitor of the H(+)-ATPase, inhibited the sodium-independent pH recovery from an acid load consistent with a H(+)-ATPase on the apical membrane. In neonatal PCT, recovery from an acid load was 0.39 +/- 0.08 pH units/min in the presence of sodium and only 0.08 pH units/min in the absence of sodium (p less than 0.05). Studies using 4 mmol/L luminal amiloride, an inhibitor of the Na+/H+ antiporter, were consistent with a larger fraction of pH recovery from an acid load in neonatal PCT being due to the Na+/H+ antiporter compared with adult PCT. Thus, maturation of the PCT involves an increase in activity of a sodium-independent proton secretory mechanism, presumably the H(+)-ATPase.