The development of the Na/H antiporter was studied in renal brush border membrane vesicles (BBMV) from fetal and adult rabbits using isotopic and fluorescent techniques. The kinetics of the antiporter studied by Na-22+ uptake revealed that the V(max) was only 25% of that in the adult; however, the K(m)'s for Na+ were not significantly different. These data were confirmed by a fluorescent assay using the pH-sensitive probe, acridine orange: the V(max) was significantly lower in the fetal BBMV. Conductive Na+ movement was estimated from amiloride-insensitive Na-22+ uptake and the rate of alkalinization induced by K+, an ion whose relative conductance was found to be similar to that of Na+. Although relative Na+ conductance was significantly greater in fetal BBMV, the lower V(max) in fetal vesicles could not be ascribed to this factor. Maternal administration of betamethasone (50-mu-g/kg intramuscularly) for 2 d before delivery significantly increased the V(max) of the antiporter to levels observed in the adult; K(m) was unaffected. Na/K ATPase activity increased fourfold after betamethasone, but the specific activities of four brush border marker enzymes and the kinetics of Na+-glucose cotransport were unchanged. These data indicate that there is a developmental increase in brush border Na/H exchange which is the result of an increase in the number and/or the turnover number of the carriers. Further, these data suggest that the postnatal increase in antiporter activity may be related to the surge in glucocorticoid concentration that occurs perinatally.
