Chen L K, Boron W F
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510.
Am J Physiol. 1995 Feb;268(2 Pt 2):F193-203. doi: 10.1152/ajprenal.1995.268.2.F193.
Monitoring intracellular absorbance spectra of the pH-sensitive dye dimethylcarboxyfluorescein we studied intracellular pH (pHi) regulation in the isolated perfused S3 segment of the rabbit proximal tubule. In the preceding study [Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F179-F192, 1995.], we demonstrated that simultaneously adding CO2/HCO3- to both lumen and bath stimulated two acid-extruding mechanisms, one dependent on luminal Na+ (a Na+/H+ exchanger) and one independent of Na+ (presumably a H+ pump). Here, we examine the effects of adding CO2/HCO3- to the lumen only or to the bath only. Over a broad pHi range, the total rate of pHi recovery from an acid load in the presence of Na+ was not increased by luminal CO2/HCO3-. On the other hand, basolateral CO2/HCO3- increased the pHi recovery rate to an even greater extent than had bilateral CO2/HCO3-. Regarding the Na(+)-independent pHi recovery mechanism, we found that luminal CO2/HCO3- failed to increase the pHi recovery rate compared with controls also studied in the absence of Na+. Neither did luminal CO2/HCO3- significantly affect the lag time between the maximal acid load and the initiation of the Na(+)-independent pHi recovery (approximately 147 vs. approximately 212 s in controls). On the other hand, adding CO2/HCO3- to only the bath substantially increased the rate of Na(+)-independent pHi recovery, which generally was greater than that observed with bilateral CO2/HCO3-. CO2/HCO3- only in the bath also reduced the lag time to approximately 51 s, which is not significantly different from the value of approximately 36 s observed with bilateral CO2/HCO3-. Our data are consistent with the hypothesis that basolateral (but not luminal) CO2/HCO3- stimulates both a luminal Na+/H+ exchanger and a luminal H+ pump.
通过监测pH敏感染料二甲基羧基荧光素的细胞内吸收光谱，我们研究了兔近端小管分离灌注S3段中的细胞内pH（pHi）调节。在之前的研究[《美国生理学杂志》268卷（肾脏液体电解质生理学37）：F179 - F192，1995年]中，我们证明同时向管腔和浴液中添加CO2/HCO3-会刺激两种酸排出机制，一种依赖于管腔Na+（一种Na+/H+交换器），另一种不依赖于Na+（可能是一种H+泵）。在此，我们研究仅向管腔或仅向浴液中添加CO2/HCO3-的影响。在较宽的pHi范围内，在有Na+存在的情况下，管腔CO2/HCO3-不会增加从酸负荷中恢复pHi的总速率。另一方面，基底外侧CO2/HCO3-使pHi恢复速率增加的程度甚至比双侧CO2/HCO3-更大。关于不依赖Na+的pHi恢复机制，我们发现与在无Na+情况下研究的对照相比，管腔CO2/HCO3-未能增加pHi恢复速率。管腔CO2/HCO3-也未显著影响最大酸负荷与不依赖Na+的pHi恢复开始之间的延迟时间（对照中约为147秒对约212秒）。另一方面，仅向浴液中添加CO2/HCO3-会显著增加不依赖Na+的pHi恢复速率，该速率通常大于双侧CO2/HCO3-时观察到的速率。仅在浴液中的CO2/HCO3-也将延迟时间缩短至约51秒，这与双侧CO2/HCO3-时观察到的约36秒的值无显著差异。我们的数据与以下假设一致，即基底外侧（而非管腔）CO2/HCO3-会刺激管腔Na+/H+交换器和管腔H+泵。
