Dixon J M, Loretz C A
J Comp Physiol B. 1986;156(6):803-11. doi: 10.1007/BF00694254.
The rate of luminal alkalinization in vitro by Gillichthys mirabilis posterior intestine as measured by a manual pH stat technique was 0.70 +/- 0.05 mu Equiv/cm2 h; acidification of the mucosal medium was never observed. The rate of HCO-3 secretion (JHCO3) was reduced by ouabain, serosally-applied DIDS, removal of serosal HCO3- and replacement of media Cl- with gluconate. HCO3- secretion was enhanced by replacement of Cl- with isethionate and unaffected by mucosal DIDS, furosemide or acetazolamide. JHCO3 was reduced at mucosal pH above or below 7.5. These results support active HCO3- secretion via a Cl-/HCO3- exchange mechanism on the basolateral membrane and a conductive exit pathway for HCO-3, H+ or OH- on the apical membrane.
通过手动pH计技术测量，奇异吉氏鱼后肠体外管腔碱化速率为0.70±0.05微当量/平方厘米·小时；从未观察到黏膜介质酸化。哇巴因、浆膜侧施加的二异丙基氟磷酸（DIDS）、去除浆膜侧碳酸氢根以及用葡萄糖酸盐替代介质中的氯离子会降低碳酸氢根分泌速率（JHCO3）。用羟乙基磺酸替代氯离子可增强碳酸氢根分泌，而黏膜侧施加DIDS、速尿或乙酰唑胺对其无影响。当黏膜pH高于或低于7.5时，JHCO3会降低。这些结果支持通过基底外侧膜上的氯离子/碳酸氢根交换机制进行主动碳酸氢根分泌，以及通过顶端膜上的碳酸氢根、氢离子或氢氧根离子传导性排出途径进行主动碳酸氢根分泌。
