PRENATAL GLUCOCORTICOIDS STIMULATE NEONATAL JUXTAMEDULLARY PROXIMAL CONVOLUTED TUBULE ACIDIFICATION
PRENATAL GLUCOCORTICOIDS STIMULATE NEONATAL JUXTAMEDULLARY PROXIMAL CONVOLUTED TUBULE ACIDIFICATION
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DOI：
10.1152/ajprenal.1991.261.5.f746
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发表时间：
1991-11-01
影响因子：
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通讯作者：
QUIGLEY, R
中科院分区：
文献类型：
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作者：
BAUM, M;QUIGLEY, R
新生动物近曲小管（PCT）吸收HCO 3的速率低于成年动物。 目前的体外微灌注研究检查了产前地塞米松（60 μ g/kg，每天给母鹿，分娩前3天）是否会加速新生儿延髓PCT酸化的成熟。 出生后48小时内研究的对照新生儿的尿液pH值为7.06 +/- 0.15，尿液HCO 3浓度为34.3 +/- 7.0 meq/l。 接受地塞米松的动物的尿液pH为6.47 +/- 0.11，尿液HCO 3浓度为10.1 +/- 4.0 meq/l，两者均显著低于对照组（P < 0.01）。 在体外灌注的骨髓PCTs中，对照组的体积吸收为0.27 +/- 0.03 nl.mm-1.min-1，对照组为0.39 +/- 0.02 nl. mm-1.min-1（P < 0.05）。 地塞米松组HCO 3吸收受到刺激（52.6 +/- 4.6 vs. 34.1 +/- 6.3 pmol.mm-1.min-1，P < 0.05）;然而，葡萄糖转运没有受到显著影响（地塞米松组24.8 +/- 1.3 vs.对照组21.5 +/- 3.5 pmol.mm-1.min-1）。 使用2 '，7'-双（羧乙基）-5（6）-羧基荧光素测量细胞内pH以检查产前地塞米松是否刺激顶端Na+-H+反向转运体和基底外侧Na（HCO 3）3同向转运体。 对照组心尖Na+-H+逆向转运体质子通量为108.5 +/- 14.2 pmol.mm-1.min-1，地塞米松组为250.7 +/- 31.3 pmol.mm-1.min-1（P < 0.001）。 对照组基底外侧Na（HCO 3）3同向转运体质子通量为106.1 +/- 10.0 pmol.mm-1.min-1，地塞米松组为202.6 +/- 17.8 pmol.mm-1.min-1（P < 0.001）。 因此，产前地塞米松通过增加顶端Na+-H+反向转运体和基底外侧Na（HCO 3）3同向转运体活性，部分地刺激延髓PCTHCO 3吸收。 这些数据与糖皮质激素在近端肾小管成熟中的作用一致。
The rate of neonatal proximal convoluted tubule (PCT) HCO3 absorption is lower than that of adult animals. The present in vitro microperfusion study examined whether prenatal dexamethasone (60-mu-g/kg daily to the doe for 3 days before delivery) would accelerate the maturation of neonatal juxtamedullary PCT acidification. Control neonates studied within 48 h of birth had a urine pH of 7.06 +/- 0.15 and a urine HCO3 concentration of 34.3 +/- 7.0 meq/l. Animals receiving dexamethasone had a urine pH of 6.47 +/- 0.11 and a urine HCO3 concentration of 10.1 +/- 4.0 meq/l, both of which were significantly lower than control (P < 0.01). In juxtamedullary PCTs perfused in vitro, volume absorption was 0.27 +/- 0.03 nl.mm-1.min-1 in controls and 0.39 +/- 0.02 nl. mm-1.min-1 in dexamethasone-treated animals (P < 0.05). HCO3 absorption was stimulated in the dexamethasone group (52.6 +/- 4.6 vs. 34.1 +/- 6.3 pmol.mm-1.min-1, P < 0.05); however, glucose transport was not significantly affected (24.8 +/- 1.3 in dexamethasone vs. 21.5 +/- 3.5 pmol.mm-1.min-1 in controls). Intracellular pH was measured using 2',7'-bis(carboxyethyl)-5(6)-carboxyflourescein to examine whether prenatal dexamethasone stimulated the apical Na+-H+ antiporter and the basolateral Na(HCO3)3 symporter. Apical Na+-H+ antiporter proton flux was 108.5 +/- 14.2 pmol.mm-1.min-1 in the control group and 250.7 +/- 31.3 pmol.mm-1.min-1 in the dexamethasone group (P < 0.001). Basolateral Na(HCO3)3 symporter proton flux was 106.1 +/- 10.0 pmol.mm-1.min-1 in control animals and 202.6 +/- 17.8 pmol.mm-1.min-1 in the dexamethasone group (P < 0.001). Thus prenatal dexamethasone stimulates juxtamedullary PCTHCO3 absorption in part by increasing apical Na+-H+ antiporter and basolateral Na(HCO3)3 symporter activity. These data are consistent with a role for glucocorticoids in proximal tubular maturation.