Igarashi Y, Aperia A, Larsson L, Zetterström R
Am J Physiol. 1983 Aug;245(2):F232-7. doi: 10.1152/ajprenal.1983.245.2.F232.
The mechanism by which betamethasone induces Na-K-ATPase activity in developing tissue was studied in homogenates of proximal tubular cells from 10-day-old rats. A significant increase in Na-K-ATPase activity occurred after 5 micrograms . 100 g-1 . 12 h-1 X 2 beta-methasone and a maximal increase after 15-60 micrograms . 100 g-1 . 12 h-1 X 2. Following a single dose of 60 micrograms . 100 g-1 betamethasone Na-K-ATPase activity increased significantly after 16 h and maximally after 24-30 h. The 16-h time lag suggests that betamethasone does not act only directly on Na-K-ATPase synthesis. Betamethasone 60 micrograms . 100 g-1 increases Na-K-ATPase activity significantly in kidneys in which glomerular filtration rate is reduced by ureteral ligation, but the increase is significantly less pronounced than in kidneys with intact ureters, suggesting that the induction is not mediated only by alterations in sodium supply. Twenty-four hours after 10-60 micrograms . 100 g-1 betamethasone there was no significant increase in glucose-6-phosphatase and Mg-ATPase activity in 10-day-old rats or in Na-K-ATPase activity in 40-day-old rats. The basal and lateral cell membranes of the proximal tubular cells were not significantly increased 24 h after 60 micrograms . 100 g-1 betamethasone. Accordingly, structural development is not a prerequisite for enzymatic differentiation.
在10日龄大鼠近端肾小管细胞匀浆中研究了倍他米松在发育组织中诱导钠钾-ATP酶活性的机制。给予5微克·100克⁻¹·12小时⁻¹×2倍他米松后,钠钾-ATP酶活性显著增加,给予15 - 60微克·100克⁻¹·12小时⁻¹×2后活性达到最大增加。单次给予60微克·100克⁻¹倍他米松后,16小时后钠钾-ATP酶活性显著增加,24 - 30小时后达到最大。16小时的时间滞后表明倍他米松并非仅直接作用于钠钾-ATP酶的合成。60微克·100克⁻¹倍他米松可使输尿管结扎导致肾小球滤过率降低的肾脏中的钠钾-ATP酶活性显著增加,但增加幅度明显小于输尿管完整的肾脏,这表明诱导作用并非仅由钠供应的改变介导。给予10 - 60微克·100克⁻¹倍他米松24小时后,10日龄大鼠的葡萄糖-6-磷酸酶和镁-ATP酶活性以及40日龄大鼠的钠钾-ATP酶活性均无显著增加。给予60微克·100克⁻¹倍他米松24小时后,近端肾小管细胞的基底侧细胞膜无显著增加。因此,结构发育不是酶分化的先决条件。