McColl K E, Buchanan N M, Laferla G, Hearns J, Buchanan K, Crean G P
Gut. 1987 Apr;28(4):455-9. doi: 10.1136/gut.28.4.455.
As calcium is important in the regulation of gastric acid secretion and gastrin release, we have examined the effect of the calcium antagonist nifedipine on these processes in man. Nifedipine 30 mg orally inhibited basal acid output by 37% (p less than 0.025) and that stimulated by low infusion rates of pentagastrin--that is, 0.031 and 0.062 microgram/kg/h by 44% (p = 0.05) and 39% (p less than 0.02) respectively. On increasing the pentagastrin infusion rate the inhibition was surmounted suggesting it was competitive in type. Nifedipine did not affect basal or Oxo meal stimulated gastrin concentrations in normal volunteers nor did it affect resting serum gastrin or calcium stimulated increase in gastrin in a single patient with Zollinger-Ellison syndrome. These findings are consistent with the transmembrane flux of calcium ions being involved in basal and pentagastrin stimulated acid secretion in man.
由于钙在胃酸分泌和胃泌素释放的调节中起重要作用,我们研究了钙拮抗剂硝苯地平对人体这些过程的影响。口服30毫克硝苯地平可使基础酸排出量降低37%(p<0.025),并使由低剂量五肽胃泌素输注(即0.031和0.062微克/千克/小时)刺激的酸排出量分别降低44%(p=0.05)和39%(p<0.02)。随着五肽胃泌素输注速率的增加,这种抑制作用被克服,提示其为竞争性抑制类型。硝苯地平对正常志愿者的基础或试餐刺激的胃泌素浓度无影响,对一名卓-艾综合征患者的静息血清胃泌素或钙刺激的胃泌素增加也无影响。这些发现与钙离子的跨膜通量参与人体基础和五肽胃泌素刺激的酸分泌一致。