Ko S B, Naruse S, Kitagawa M, Ishiguro H, Murakami M, Hayakawa T
Internal Medicine II, Nagoya University School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
Am J Physiol. 1999 Jul;277(1):G48-54. doi: 10.1152/ajpgi.1999.277.1.G48.
The effects of arginine vasopressin (AVP) on pancreatic ductal secretion were studied in guinea pigs. In the isolated vascularly perfused pancreas, AVP reduced secretin-stimulated fluid secretion and increased the vascular resistance when the perfusion rate was held constant. In the isolated interlobular duct segments, AVP inhibited secretin-stimulated fluid secretion, indicating the direct inhibitory action of AVP on the duct cells. AVP affected neither the basal nor the secretin-induced cAMP productions, suggesting that AVP inhibits the fluid secretion at a point distal to the production of cAMP. AVP increased intracellular Ca(2+) concentration (Ca(2+)) in the absence of extracellular Ca(2+). When Ca(2+) was elevated by the application of thapsigargin, AVP caused a rapid decrease in Ca(2+). AVP seems to activate both Ca(2+) release from intracellular stores and Ca(2+) efflux across the plasma membrane, but its relation to the inhibition of fluid secretion remains to be clarified. It is concluded that AVP directly inhibits secretin-stimulated ductal fluid secretion in the guinea pig pancreas.
