Department of Internal Medicine, Institute of Digestive Disease and Nutrition, Korea University College of Medicine, Seoul, Korea
Corresponding author:
Chang Duck Kim,
ABSTRACT
Background/Aims: Nitric oxide (NO) is a noxious, unstable vasodilator formed by NO synthase (NOS) from L-arginine (L-Arg) in various cells but its role in the control of pancreatic exocrine secretion has not been fully examined. This study was designed to determine the role of endogenous NO in the control of exocrine pancreas on resting and cholecystokinin (CCK)-stimulated state. Methods: Thirty-two male Sprague-Dawley rats (250-300 g/weight) were prepared with jugular vein cannulation and pyloric ligation. Pancreatic duct was cannulated with PE-10 tube and bile duct was cannulated with PE-10 tube for diverging of bile juice. For a resting state and CCK stimulated state, each rat recieved an intravenous (lV) infusion of 0.5M Nacl (1.56 ml/hr) or CCK (50-500 mg/kg/hr) for 1 hour, respectively. L-NAME (5 mg/kg) and L-Name (5 mg/kg/hr) plus L-arginine (100 mg/kg) were administered in bolus at 30 minutes after the onset of NaCl or CCK infusion. Results: In resting state, the pancreatic secretory volume and protein output were significantly suppressed by L-NAME (20.8±2.7 vs 14.7±2.6 μl/30 min, 110±12 vs 60±8 μg/30 min, respectively). The suppression of pancreatic volume by L-NAME was reversed by IV administration of L-NAME plus L-arginine. In CCK-stimulated state at 50 and 100 ng/kg/hr, the pancreatic volume and protein output were not changed by IV administration of L-NAME, but the pancreatic secretory volume and protein output were significantly decreased by L-NAME in 500 ng/kg/hr of CCK. The pancreatic secretory volume and protein output were also increased by IV administration of L-NAME plus L-arginine in 500 ng/kg/hr of CCK. Conclusion: These results suggest that nitric oxide involve in resting exocrine pancreatic secretion and CCK-stimulated state at 500 ng/kg/hr, but not in 50 and 100 ng/kg/hr of CCK.