Uhlemann E R, Robberecht P, Gardner J D
Gastroenterology. 1979 May;76(5 Pt 1):917-25.
In dispersed acini prepared from guinea pig pancreas, ethanol inhibited the increase in amylase secretion caused by cholecystokinin, carbachol, secretin, or vasoactive intestinal peptide. Ethanol did not alter binding of [125I] vasoactive intestinal peptide to pancreatic acinar cells or the inhibition of binding cause by secretin or vasoactive intestinal peptide. Ethanol potentiated the increase in adenylate cyclase activity and cellular adenosine 3':5'-monophosphate caused by secretin or vasoactive intestinal peptide. This potentiating action was reversible and could also be detected with straight-chain alcohols having fewer than seven carbon atoms. At sufficiently high concentrations, straight-chain alcohols having more than two carbon atoms inhibited the action of secretin or vasoactive intestinal peptide on adenylate cyclase activity, and this and this action was irreversible.
在从豚鼠胰腺制备的分散腺泡中,乙醇抑制了由胆囊收缩素、卡巴胆碱、促胰液素或血管活性肠肽引起的淀粉酶分泌增加。乙醇并未改变[125I]血管活性肠肽与胰腺腺泡细胞的结合,也未改变促胰液素或血管活性肠肽对结合的抑制作用。乙醇增强了促胰液素或血管活性肠肽引起的腺苷酸环化酶活性增加以及细胞内3':5'-环磷酸腺苷水平升高。这种增强作用是可逆的,并且具有少于七个碳原子的直链醇也能检测到这种作用。在足够高的浓度下,具有两个以上碳原子的直链醇抑制促胰液素或血管活性肠肽对腺苷酸环化酶活性的作用,并且这种作用是不可逆的。