Pathophysiological and possible physiological roles of kinins in the pancreas.

The i.v. infusion of a low dose of the cholecystokinin agonist caerulein elicited a sustained secretion of amylase into the biliopancreatic duct of rats. Pretreatment with the bradykinin antagonist icatibant (Hoe-140) had no effect on unstimulated amylase release and did not affect caerulein-induced amylase secretion. An i.v. infusion of bradykinin in doses not producing a pancreatic oedema elicited an increase in pancreatic juice production lasting 20-40 min after the end of the infusion. This pro-secretory effect was also visible at higher doses in captopril-pretreated rats producing an oedema similar to that observed in caerulein-induced pancreatitis. Using the Monastral blue method, it was found that the kininase II blocker captopril induced an opening of endothelial gaps in pancreatic capillaries. This effect was blocked by icatibant suggesting that kinins are formed in the pancreas under basal conditions. Thus, kinins appear not to be involved in the regulation of the production of digestive enzymes. However, kinins may have a modulatory role in the production of pancreatic juice and in the microcirculatory regulation in the pancreas.