TY - JOUR
T1 - Developmental changes in rabbit juxtamedullary proximal convoluted tubule acidification
AU - Baum, M.
PY - 1992/4
Y1 - 1992/4
N2 - 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 NH4CI.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 0.2S ± 0.05 in the absence of sodium (p< 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 < 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.
AB - 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 NH4CI.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 0.2S ± 0.05 in the absence of sodium (p< 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 < 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.
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U2 - 10.1203/00006450-199204000-00021
DO - 10.1203/00006450-199204000-00021
M3 - Article
C2 - 1315022
AN - SCOPUS:0026580732
SN - 0031-3998
VL - 31
SP - 411
EP - 414
JO - Pediatric Research
JF - Pediatric Research
IS - 4
ER -