Cremaschi D, Meyer G, Rossetti C
J Physiol. 1983 Feb;335:51-64. doi: 10.1113/jphysiol.1983.sp014518.
The stimulating effect of external HCO3- on Na+ salt transport has been examined in rabbit and guinea-pig gall-bladder by electrophysiological methods, as a sequel to a previous study carried out by radiochemical techniques. At steady state, cell K+ activity was found to be significantly reduced in the presence of HCO3-, whereas cell Na+ activity significantly increased; in parallel the apical membrane p.d. was depolarized; K+ equilibrium potential was higher than membrane p.d. in every case. The apical p.d. dependence on K+ was unaffected by HCO3-, but in the guinea-pig it was affected by Cl-. Rapid increases in HCO3- concentration on the luminal side caused a depolarization of the apical p.d. of the guinea-pig within about 30 sec, an effect that did not occur if the tissue was pre-treated with 10(-4) M-acetazolamide; the epithelial resistance and apical/basolateral resistance ratio were unchanged in all cases. The primary action of HCO3- is confirmed to be on the apical membrane; an HCO3- conductance does not seem to be present at this level, either in the rabbit or guinea-pig, nor does HCO3- affect Na+ influx through the apical conductive pathway, so that all the stimulating effects of the anion are confirmed to be on the neutral transports of Na+ salts; in spite of this, the apical electromotive force is modified due to the changed cell K+ activity. The rapid depolarization caused by the anion in the guinea-pig is in agreement with an HCO3- electrogenic secretion and/or a basolateral conductance for the anion. Polyelectrolyte dissociation from protons increases in the absence of external HCO3-: the negative charges are mainly counterbalanced by bound Na+ in the rabbit and by free K+ in the guinea-pig. K+ leakage from the cell into the lumen is calculated to be minimal in the rabbit and all K+ lost could be reabsorbed through the paracellular pathways; K+ efflux to the subepithelial layer via conductive routes is insufficient to account for the over-all K+ efflux.
继先前采用放射化学技术开展的一项研究之后，已通过电生理方法对兔和豚鼠胆囊中外源性HCO₃⁻对钠盐转运的刺激作用进行了研究。在稳态下，发现存在HCO₃⁻时细胞K⁺活性显著降低，而细胞Na⁺活性显著增加；与此同时，顶端膜电位去极化；在每种情况下K⁺平衡电位均高于膜电位。顶端电位对K⁺的依赖性不受HCO₃⁻影响，但在豚鼠中受Cl⁻影响。管腔侧HCO₃⁻浓度的快速增加在约30秒内导致豚鼠顶端电位去极化，如果组织用10⁻⁴M乙酰唑胺预处理则不会出现这种效应；在所有情况下上皮电阻以及顶端/基底外侧电阻比值均未改变。证实HCO₃⁻的主要作用是作用于顶端膜；在兔或豚鼠中该水平似乎均不存在HCO₃⁻电导，HCO₃⁻也不影响通过顶端传导途径的Na⁺内流，因此该阴离子的所有刺激作用均证实是对钠盐的中性转运；尽管如此，由于细胞K⁺活性改变，顶端电动势发生了改变。该阴离子在豚鼠中引起的快速去极化与HCO₃⁻的电致分泌和/或该阴离子的基底外侧电导一致。在没有外源性HCO₃⁻的情况下质子的聚电解质解离增加：在兔中负电荷主要由结合的Na⁺平衡，在豚鼠中由游离的K⁺平衡。据计算，兔中K⁺从细胞漏入管腔的量极少，所有丢失的K⁺均可通过细胞旁途径重吸收；通过传导途径向上皮下层的K⁺外流不足以解释总的K⁺外流。
