Liu F Y, Cogan M G
Cardiovascular Research Institute, University of California, San Francisco.
Am J Physiol. 1990 Sep;259(3 Pt 2):F451-7. doi: 10.1152/ajprenal.1990.259.3.F451.
Using in vivo microperfusion in the proximal convoluted tubule (PCT) of the Munich-Wistar rat, we assessed the impact of raising intracellular calcium concentration on bicarbonate transport and its regulation by angiotensin II. Luminal perfusion with the calcium ionophore A23187 caused a dose-dependent increase in S1 PCT bicarbonate absorption, with a maximal change of 60 peq.mm-1.min-1. Subsequent addition of phorbol ester (PMA) after A23187 further increased transport but to a level no higher than previously shown with PMA alone, and A23187 was nonstimulatory when added after PMA. These results suggest that intracellular calcium affects the same pathway as protein kinase C in stimulating proximal acidification. Pretreatment with A23187 (+/- PMA) attenuated by approximately one-third the bicarbonate absorptive response in the S1 PCT usually observed after angiotensin II administration. A23187 had similar actions, but of smaller magnitude, in the S2 PCT. In conclusion, a rise in intracellular calcium increases bicarbonate absorption in the S1 and S2 PCT in vivo.
利用慕尼黑-威斯塔大鼠近端曲管(PCT)的体内微灌注技术,我们评估了提高细胞内钙浓度对碳酸氢盐转运及其受血管紧张素II调节的影响。用钙离子载体A23187进行管腔灌注导致S1段PCT碳酸氢盐吸收呈剂量依赖性增加,最大变化为60 peq·mm-1·min-1。在A23187之后随后添加佛波酯(PMA)进一步增加了转运,但不高于单独使用PMA时的水平,且在PMA之后添加A23187无刺激作用。这些结果表明,细胞内钙在刺激近端酸化时影响与蛋白激酶C相同的途径。用A23187(±PMA)预处理可使通常在给予血管紧张素II后观察到的S1段PCT碳酸氢盐吸收反应减弱约三分之一。A23187在S2段PCT中具有类似作用,但程度较小。总之,细胞内钙升高会增加体内S1和S2段PCT的碳酸氢盐吸收。