Seki G, Taniguchi S, Uwatoko S, Suzuki K, Kurokawa K
First Department of Internal Medicine, Tokyo University School of Medicine, Japan.
Pflugers Arch. 1993 Apr;423(1-2):7-13. doi: 10.1007/BF00374954.
The effect of parathyroid hormone (PTH) on acid/base transport in isolated rabbit renal proximal tubule S3 segment was investigated with double-barreled and conventional microelectrodes. PTH (10 nM) induced a small depolarization and enhanced the initial rates of cell pH (pHi) increase and cell Cl- ([Cl-]i) decrease in response to bath Cl- removal by 28.0 +/- 2.1% and 31.0 +/- 6.4% respectively. The calculated initial HCO3- influx to bath Cl- removal was also enhanced by 28%. On the other hand, PTH reduced the initial rate of pHi decrease to luminal Na+ removal in the absence of HCO3-/CO2 by 20.4 +/- 3.9%. The PTH-induced depolarization was not accompanied with changes in steady-state pHi or [Cl-]i levels, but was greatly attenuated in the presence of ouabain (0.1 mM). Either dibutyryl-cAMP (0.1 mM) plus theophylline (1 mM) or forskolin (10 microM) alone could reproduce all the effects of PTH. These results indicate that (a) PTH inhibits the luminal Na+/H+ exchanger but stimulates the basolateral Cl-/HCO3- exchanger in the S3 segment; (b) the PTH-induced depolarization largely results from inhibition of Na+/K(+)-ATPase and (c) all these effects are at least partly mediated by a cAMP-dependent mechanism.
采用双管微电极和传统微电极研究了甲状旁腺激素（PTH）对离体兔肾近端小管S3段酸碱转运的影响。PTH（10 nM）可引起轻微去极化，并增强细胞pH（pHi）升高和细胞Cl-（[Cl-]i）降低的初始速率，对去除浴液中的Cl-反应时，分别增加28.0±2.1%和31.0±6.4%。计算得出的去除浴液中Cl-时HCO3-的初始内流也增加了28%。另一方面，在不存在HCO3-/CO2的情况下，PTH使pHi降低至管腔Na+去除的初始速率降低20.4±3.9%。PTH诱导的去极化不伴有稳态pHi或[Cl-]i水平的变化，但在哇巴因（0.1 mM）存在时大大减弱。二丁酰-cAMP（0.1 mM）加茶碱（1 mM）或单独的福斯可林（10 μM）均可重现PTH的所有作用。这些结果表明：（a）PTH抑制S3段管腔Na+/H+交换体，但刺激基底外侧Cl-/HCO3-交换体；（b）PTH诱导的去极化主要源于对Na+/K(+)-ATP酶的抑制；（c）所有这些作用至少部分由cAMP依赖性机制介导。
