Maturation of proximal tubular acidification

Abstract

Neonatal juxtamedullary proximal convoluted tubules (PCTs) transport bicarbonate at one-third the rate of adult rabbit PCTs. The lower rate of bicarbonate transport could be due to a greater permeability of the neonatal PCT to bicarbonate or to a lower rate of active bicarbonate transport. This review discusses potential factors which could result in a lower rate of bicarbonate transport by the neonatal PCT. In isolated perfused PCT, bicarbonate permeability is lower in neonatal than adult PCT, and thus it does not account for the lower rate of bicarbonate transport in neonatal PCT. In the adult PCT, apical proton secretion occurs via the Na+/H+ antiporter and H(+)-ATPase; basolateral bicarbonate exit occurs via the Na(HCO3)3 symporter. The activity of transporters can be ascertained by measuring intracellular pH with the fluorescent dye BCECF. Apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter activity are all significantly lower in neonatal PCT. The factors which stimulate PCT maturation are unknown, however glucocorticoids have been postulated to play an important role in this process. Administration of dexamethasone to pregnant does results in higher rates of PCT volume absorption, bicarbonate transport, Na+/H+ antiporter and Na(HCO3)3 symporter activities than in PCT from vehicle-treated controls. Thus, the lower rate of neonatal PCT bicarbonate transport is due to lower activities of the apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter. Glucocorticoids may be an important factor in the maturation of PCT acidification.