Lewis J J, Goldenring J R, Asher V A, Modlin I M
Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.
Biochem Biophys Res Commun. 1989 Sep 15;163(2):667-73. doi: 10.1016/0006-291x(89)92275-4.
The direct inhibition of secretion by pancreastatin was investigated in rabbit isolated parietal cells. Pancreastatin exerted no influence on basal aminopyrine uptake. Pancreastatin inhibited histamine stimulated aminopyrine uptake through a decrease in intracellular cAMP. Pancreastatin inhibition of histamine stimulated uptake was blocked in the presence of pertussis toxin. Pancreastatin also inhibited the carbachol stimulated increase in aminopyrine accumulation. However, the effects of pancreastatin on carbachol stimulation were not reversed by pertussis toxin. Pancreastatin did not alter the carbachol induced increase in cytosolic free calcium. Thus, pancreastatin appears to inhibit parietal cell signal transduction at multiple points along the second messenger pathways.
在兔离体壁细胞中研究了胰抑制素对分泌的直接抑制作用。胰抑制素对基础氨基比林摄取没有影响。胰抑制素通过降低细胞内cAMP来抑制组胺刺激的氨基比林摄取。在百日咳毒素存在的情况下,胰抑制素对组胺刺激摄取的抑制作用被阻断。胰抑制素也抑制了卡巴胆碱刺激引起的氨基比林蓄积增加。然而,百日咳毒素并不能逆转胰抑制素对卡巴胆碱刺激的作用。胰抑制素没有改变卡巴胆碱诱导的细胞溶质游离钙增加。因此,胰抑制素似乎在第二信使途径的多个点上抑制壁细胞信号转导。