| [ Summary ] |
Nitric oxide synthase (NOS)-immunoreactivity and/or NADPH-diaphorese-immunoreactivity were localized in nerve fibers, nerve cell bodies and the vascular endothelium in the exocrine pancreas, and in alpha cells and delta cells in the endocrine pancreas. But they were not detectable in exocrine cells and beta cells in the pancreas. NO failed to affect basal and secretagogue stimulated amylase release in the dispersed acini. NO playsa permissive role in spontaneous and CCK- or VIP- and meal-stimulated pancreatic secretion, perhaps via the maintenance and increase of adequate blood flow. In cerulein-induced pancreatitis, NO produced from CNOS might attenuate pancreatic injury. Inhibition of nuclear factor-kappa B activation caused suppression of iNOS and improved the survival of rats with severe necrotizing pancreatitis which, showed an increase in serum NOx. Endogenous NO inhibited glucose-induction and insulin secretion. Production of NO, resulting from the expression of the cytokine-inducible isoforms of NOS is thought to be important in initiating or maintaining apoptosis and necrosis of beta cells associated with autoimmune diabetes. |