Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Mol Biol Rep. 2010 Mar;37(3):1329-33. doi: 10.1007/s11033-009-9511-9. Epub 2009 Mar 21.
The KCNQ1 channel is abundantly expressed in the gastric parietal cells. Although the functional coupling of KCNQ1 with the H(+)/K(+)-ATPase has already been confirmed on the basis of pharmacological kinetics, the effect of a KCNQ1 loss-of-function mutation on gastric acidification remains unclear. In this study, parietal cells and gastric glands from both C57BL/6 J mice (normal control) and J343 mice (mice with a KCNQ1 loss-of-function mutation) were isolated to study the effects of KCNQ1 on gastric acidification. We found that the mutation limited intracellular acidification of parietal cells and H(+) secretion of the stomach in response to histamine. Thus, a KCNQ1 loss-of-function mutation may impair gastric acid secretion.
KCNQ1 通道在胃壁细胞中大量表达。尽管 KCNQ1 与 H(+)/K(+)-ATP 酶的功能偶联已经基于药理学动力学得到证实,但 KCNQ1 功能丧失突变对胃酸分泌的影响仍不清楚。在这项研究中,我们从 C57BL/6 J 小鼠(正常对照)和 J343 小鼠(KCNQ1 功能丧失突变小鼠)中分离出壁细胞和胃腺,以研究 KCNQ1 对胃酸分泌的影响。我们发现,该突变限制了组胺刺激下壁细胞的细胞内酸化和胃内 H(+)分泌。因此,KCNQ1 功能丧失突变可能会损害胃酸分泌。