Suzuki Y, Kaneko K, Maruyama M, Hayashi H
Laboratory of Physiology, School of Food and Nutritional Science, University of Shizuoka, Japan.
Jpn J Physiol. 1994;44 Suppl 2:S305-7.
In guinea pig distal colon, H+ secretion into the lumen due to the apical ouabain-sensitive H+, K(+)-ATPase activity is associated with HCO3- exit into the serosa. This study aimed at elucidating (1) the transport mechanism of HCO3- exit across the basolateral membrane and (2) the relation of lactate release to the H+, K(+)-ATPase activity, in isolated mucosae mounted in Ussing chamber. The HCO3- exist across the basolateral membrane depended on the serosal Cl-. 4,4'-Diisothiocyanostilbene- anostilbene-2,2'-disulfonic acid (DIDS) applied to the serosal side reduced the rate of HCO3- exit across the basolateral membrane. The lactate was released to the serosal side, but not to the luminal side. The serosal lactate appearance was abolished when the apical H+, K(+)-ATPase was inhibited by luminal ouabain. These results suggest that HCO3- exit across the basolateral membrane is mediated by a DIDS-sensitive Cl-/HCO3- exchange. In addition, the lactic acid production appears to be coupled to the apical H+, K(+)-ATPase activity.
在豚鼠远端结肠中,由于顶端哇巴因敏感的H⁺,K⁺-ATP酶活性导致的H⁺分泌到肠腔中与HCO₃⁻进入浆膜有关。本研究旨在阐明(1)HCO₃⁻跨基底外侧膜排出的转运机制,以及(2)在置于尤斯灌流小室中的分离黏膜中乳酸释放与H⁺,K⁺-ATP酶活性的关系。HCO₃⁻跨基底外侧膜的排出依赖于浆膜侧的Cl⁻。应用于浆膜侧的4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)降低了HCO₃⁻跨基底外侧膜的排出速率。乳酸释放到浆膜侧,而不是肠腔侧。当顶端H⁺,K⁺-ATP酶被肠腔哇巴因抑制时,浆膜侧乳酸的出现被消除。这些结果表明,HCO₃⁻跨基底外侧膜的排出是由DIDS敏感的Cl⁻/HCO₃⁻交换介导的。此外,乳酸的产生似乎与顶端H⁺,K⁺-ATP酶活性相关。