Hirschowitz B I, Fong J
Am J Physiol. 1983 Dec;245(6):G739-44. doi: 10.1152/ajpgi.1983.245.6.G739.
The final step in acid secretion is believed to result from the H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the lumen. To study the K+ secretion we used Picoprazole and insulin separately and together to inhibit gastric secretion stimulated in gastric fistula dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and volume with a rise in K+ concentration [( K+]) to 20-25 meq/l. Insulin alone inhibited acid output to the same extent as Picoprazole but with a marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not alter inhibition of H+ but prevented the large decrease in gastric juice [K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter the effects of the inhibitor. Pepsin secretion after insulin was delayed by Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser extent than acid. We concluded that insulin affects gastric H+ and K+ secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole affects pepsin secretion probably indirectly via its effect on the parietal cell, where its action is quite consistent with an effect limited to inhibition of the H+-K+-ATPase of the parietal cell.
胃酸分泌的最后一步被认为是由于壁细胞中H⁺-K⁺-ATP酶介导的H⁺与管腔中的K⁺交换所致。为了研究K⁺分泌，我们分别单独使用吡考拉唑和胰岛素，并将它们联合使用，以抑制组胺（100微克/千克·小时⁻¹）刺激的胃瘘犬的胃液分泌。吡考拉唑是一种取代苯并咪唑（750毫克/千克），可降低胃内H⁺浓度和胃液量，同时K⁺浓度[（K⁺）]升高至20 - 25毫当量/升。单独使用胰岛素抑制胃酸分泌的程度与吡考拉唑相同，但[K⁺]显著下降。与吡考拉唑联合使用的胰岛素（0.6单位/千克）并没有改变对H⁺的抑制作用，但防止了胃液[K⁺]的大幅下降。在给予吡考拉唑1小时后注射氯化钾（1毫当量/千克）并没有改变抑制剂的作用。吡考拉唑延迟了胰岛素作用后的胃蛋白酶分泌，而在输注氯贝胆碱（80微克/千克·小时⁻¹）期间，胃蛋白酶分泌减少的时间较短，程度也比胃酸分泌减少的程度小。我们得出结论，胰岛素通过一种与H⁺-K⁺-ATP酶无关的机制影响胃H⁺和K⁺分泌，并且吡考拉唑可能通过其对壁细胞的作用间接影响胃蛋白酶分泌，其作用与仅限于抑制壁细胞H⁺-K⁺-ATP酶的作用相当一致。
