Knobloch S F, Diener M, Rummel W
Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg/Saar (F.R.G.).
Regul Pept. 1989 Apr;25(1):75-85. doi: 10.1016/0167-0115(89)90250-4.
The effects of two hormones, vasopressin and somatostatin (SOM), on ion secretion in rat colon descendens were compared. Three modes for induction of epithelial secretion were used: neuronally mediated secretion due to electric field stimulation (EFS), Ca2+-dependent secretion elicited by carbachol, and cAMP-dependent secretion evoked either by a receptor-mediated mechanism elicited by vasoactive intestinal peptide (VIP) or by a direct activation of the adenylate cyclase by means of forskolin. Somatostatin inhibited ion secretion evoked by EFS (55-65%), carbachol (80%) and VIP (95%) in a dose-dependent manner. Maximal inhibition by SOM was observed at 10(-7) M. Somatostatin had, however, no effect on the secretory response to forskolin. The inhibition of the VIP effect could be attenuated by pretreatment with pertussis toxin. In contrast, vasopressin in concentrations as low as 0.025-0.25 U/liter decreased the secretory effects of EFS (55-75%) and carbachol (85%), but had no effect on cAMP-dependent secretion elicited either by VIP or forskolin. The results suggest that the antisecretory effect of vasopressin is mediated only by a block in the Ca2+ pathway, whereas SOM inhibits Ca2+-dependent secretion as well as receptor-mediated cAMP-dependent secretion. The interaction with the cAMP pathway is located at the step between stimulation of the receptor and activation of the adenylate cyclase and probably involves an Ni-protein.
