TY - JOUR
T1 - Maturational effects of glucocorticoids on neonatal brush-border membrane phosphate transport
AU - Arar, M.
AU - Levi, M.
AU - Baum, M.
PY - 1994/4
Y1 - 1994/4
N2 - Previous studies have implicated glucocorticoids as an important factor in the postnatal maturational increase in proximal tubule volume absorption, Na+/H+ antiporter, Na(HCO3)3 symporter, and Na+-K+-ATPase activity. The present study examined whether glucocorticoids are also a potentially important factor in the maturational decrease in proximal tubule phosphate transport. Renal BBMs were prepared from neonatal rabbits who received dexamethasone (10 μg/100 g body weight) or vehicle. Brush-border membrane vesicles from dexameth-asone-treated neonates had a lower rate of Na-phosphate cotransport than controls (50.8 ± 3.6 versus 29.2 ± 2.6 pmol 32Pi/10 s/mg protein, p < 0.001). This decrease was due to a decrease in the Vmax with no change in the affinity of the transporter for phosphate. The dexamethasone-induced decrease in BBM Na-phosphate transport was not due to a reduction in transporters as assayed by phosphate-protectable Na-dependent equilibrium binding of phos-phonoformic acid. Dexamethasone treatment caused an increase in the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene and trimethylammonium-l,6-diphenyl-1,3,5-hexatriene (i.e. a decrease in membrane fluidity). Brush-border membranes from dexamethasone-treated neonates had a decrease in sphingomyelin and an increase in phosphatidylcholine and phosphatidylinositol content but no change in cholesterol or total phospholipid content. These data are consistent with glucocorticoids playing a role in the postnatal maturational decrease in proximal tubule phosphate transport by altering membrane characteristics.
AB - Previous studies have implicated glucocorticoids as an important factor in the postnatal maturational increase in proximal tubule volume absorption, Na+/H+ antiporter, Na(HCO3)3 symporter, and Na+-K+-ATPase activity. The present study examined whether glucocorticoids are also a potentially important factor in the maturational decrease in proximal tubule phosphate transport. Renal BBMs were prepared from neonatal rabbits who received dexamethasone (10 μg/100 g body weight) or vehicle. Brush-border membrane vesicles from dexameth-asone-treated neonates had a lower rate of Na-phosphate cotransport than controls (50.8 ± 3.6 versus 29.2 ± 2.6 pmol 32Pi/10 s/mg protein, p < 0.001). This decrease was due to a decrease in the Vmax with no change in the affinity of the transporter for phosphate. The dexamethasone-induced decrease in BBM Na-phosphate transport was not due to a reduction in transporters as assayed by phosphate-protectable Na-dependent equilibrium binding of phos-phonoformic acid. Dexamethasone treatment caused an increase in the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene and trimethylammonium-l,6-diphenyl-1,3,5-hexatriene (i.e. a decrease in membrane fluidity). Brush-border membranes from dexamethasone-treated neonates had a decrease in sphingomyelin and an increase in phosphatidylcholine and phosphatidylinositol content but no change in cholesterol or total phospholipid content. These data are consistent with glucocorticoids playing a role in the postnatal maturational decrease in proximal tubule phosphate transport by altering membrane characteristics.
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U2 - 10.1203/00006450-199404000-00016
DO - 10.1203/00006450-199404000-00016
M3 - Article
C2 - 8047384
AN - SCOPUS:0028331157
SN - 0031-3998
VL - 35
SP - 474
EP - 478
JO - Pediatric Research
JF - Pediatric Research
IS - 4
ER -