Xu P, Spitzer K W
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112.
Am J Physiol. 1994 Jul;267(1 Pt 2):H85-91. doi: 10.1152/ajpheart.1994.267.1.H85.
The pH-sensitive fluorescent indicator, carboxy-seminaphthorhodafluor 1 (SNARF 1) was used to assess the contribution of forward Na-independent Cl(-)-HCO3- exchange (1 external Cl- exchanged for 1 internal HCO3-) to intracellular pH (pHi) recovery from alkalosis in adult ventricular myocytes (guinea pig). Intracellular alkalosis was elicited by external application of the weak base, trimethylamine. In the absence of CO2-HCO3- (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solution) the initial rate of pHi recovery from alkalosis (pHi = 7.25-7.75) was slow and independent of pHi, yielding an apparent net HCO3- efflux of 0.36 +/- 0.11 mM/min. In CO2-HCO3(-)-buffered solution, the initial rate of pHi recovery and net HCO3- efflux were much faster and markedly increased by raising pHi. At pHi approximately 7.25, net HCO3- efflux was approximately 2 mM/min and rose to 9 mM/min at pHi approximately 7.6. 4,4'-Diisothiocyanostilbene-2,2'-disulfonic acid (0.4 mM) decreased net HCO3- efflux by 78.1 +/- 8.9% in CO2-HCO3(-)-buffered solution. Reduction in extracellular Cl- concentration from 135 to 20 mM markedly slowed the rate of pHi recovery from alkalosis and reduced net HCO3- efflux. pHi recovery from alkalosis was unaffected by removal of external sodium or exposure to 1 mM amiloride. These results indicate that forward Na-independent Cl(-)-HCO3- exchange mediates pHi recovery from alkalosis in guinea pig ventricular myocytes.
使用对pH敏感的荧光指示剂羧基半萘并萘荧光素1（SNARF 1）来评估正向非钠依赖性Cl⁻-HCO₃⁻交换（1个胞外Cl⁻交换1个胞内HCO₃⁻）对成年豚鼠心室肌细胞碱中毒后细胞内pH（pHi）恢复的作用。通过外部施加弱碱三甲胺引发细胞内碱中毒。在不存在CO₂-HCO₃⁻（N-2-羟乙基哌嗪-N'-2-乙烷磺酸缓冲溶液）的情况下，碱中毒后pHi恢复的初始速率（pHi = 7.25 - 7.75）较慢且与pHi无关，产生的表观净HCO₃⁻外流为0.36 ± 0.11 mM/分钟。在CO₂-HCO₃⁻缓冲溶液中，pHi恢复的初始速率和净HCO₃⁻外流要快得多，并且通过提高pHi而显著增加。在pHi约为7.25时，净HCO₃⁻外流约为2 mM/分钟，在pHi约为7.6时升至9 mM/分钟。4,4'-二异硫氰基芪-2,2'-二磺酸（0.4 mM）在CO₂-HCO₃⁻缓冲溶液中使净HCO₃⁻外流降低了78.1 ± 8.9%。将细胞外Cl⁻浓度从135 mM降低到20 mM显著减慢了碱中毒后pHi恢复的速率并减少了净HCO₃⁻外流。去除外部钠或暴露于1 mM氨氯吡脒对碱中毒后pHi的恢复没有影响。这些结果表明正向非钠依赖性Cl⁻-HCO₃⁻交换介导了豚鼠心室肌细胞碱中毒后pHi的恢复。
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