HORMONAL INDUCTION OF NA-K-ATPASE IN DEVELOPING PROXIMAL TUBULAR CELLS

HORMONAL INDUCTION OF NA-K-ATPASE IN DEVELOPING PROXIMAL TUBULAR CELLS
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DOI:
10.1152/ajprenal.1981.241.4.f356
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发表时间:
1981-01-01
影响因子:
--
通讯作者:
ZETTERSTROM, R
ZETTERSTROM, R
中科院分区:
其他
文献类型:
--
作者:
APERIA, A;LARSSON, L;ZETTERSTROM, R

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大鼠肾皮质的外部150 μ m层主要由近端小管(PT)组成。在这一层中,Na-K-ATP酶(μ mol Pi.cntdot.mg蛋白质-1.cntdot.h-1)从3.45 ± 1.00 μ mol增加到3.45 ± 1.00 μ mol。0.19(SE)在10日龄大鼠(R10)中为5.90 ±。0.28在20日龄大鼠(R20)中为9.52 ±。0.42 40日龄大鼠(R40)。药理学剂量的betterin使R10、R20和R40中的Na-K-ATP酶增加至11.5 ±。1.19,13.4 .+-。0.64和13.3 ±。分别为0.60。药理学剂量的雌激素使Na-K-ATP酶增加至9.1 ±。0.46在R20中,Na-K-ATP酶降低至7.6 ±。0.39在R40中。10 μ g/100 g BW [体重]剂量的醛固酮使Na-K-ATP酶增加至8.7 ±。0.26在R20中;在40 μ g/100 g BW剂量中,它将Na-K-ATP酶增加到6.9 ±。0.35在R10中。需要剂量为80 μ g/100 g BW的醛固酮以引起R40增加至13.4 ±。0.37.从第10天到第20天用坎利酮处理增加Na-K-ATP酶。未成熟的PT细胞对激素诱导的Na-K-ATP酶特别敏感。在细胞分化的相当晚期阶段,敏感性最高。诱导作用可能是通过糖皮质激素受体介导的。
The outer 150-.mu.m layer of the renal cortex of the rat consists mainly of proximal tubules (PT). In this layer Na-K-ATPase (.mu.mol Pi.cntdot.mg protein-1.cntdot.h-1) increases from 3.45 .+-. 0.19 (SE) in 10-day-old rats (R10) to 5.90 .+-. 0.28 in 20-day-old rats (R20) to 9.52 .+-. 0.42 in 40-day-old rats (R40). Betamethasone in pharmacologic doses increases Na-K-ATPase in R10, R20, and R40 to 11.5 .+-. 1.19, 13.4 .+-. 0.64, and 13.3 .+-. 0.60, respectively. Estrogen in pharmacologic doses increases Na-K-ATPase to 9.1 .+-. 0.46 in R20 and decreases Na-K-ATPase to 7.6 .+-. 0.39 in R40. Aldosterone in a dose of 10 .mu.g/100 g BW [body wt] increases Na-K-ATPase to 8.7 .+-. 0.26 in R20; in a dose of 40 .mu.g/100 g BW it increases Na-K-ATPase to 6.9 .+-. 0.35 in R10. Aldosterone in a dose of 80 .mu.g/100 g BW is needed to cause an increase in R40 to 13.4 .+-. 0.37. Treatment with canrenone from the 10th to the 20th day increases Na-K-ATPase. The immature PT cells are particularly sensitive to hormone induction of Na-K-ATPase. The sensitivity is maximal during fairly late stages of cellular differentiation. The inductive effect is probably mediated via glucocorticoid receptors.