Preventice effects of an angiotensin converting enzyme inhibitor and a calcium antagonist on the development of spontaneous pancreatitis in salt-loaded Dahl salt-sensitive and salt-resistant rats *
Pancreatic lesions were examined histopathologically in Dahl salt-sensitive rats (DS-S) and Dahl salt-resistant rats (DS-R) fed a high-salt ( 8 % NaCl) diet from the age of 5 weeks to 11 weeks. The DS-S rats were divided into three groups ; group 1 received drinking water throughout the experimental period, group 2 received 0.001% trandolapril (antihypertensive), and group 3 received 0. 2% verapamil (antihypertensive). The DS-R rats were also divided into three groups ; group 4 received drinking water throughout the experimental period, group 5 received 0.001% trandolapril, and group 6 received 0. 2% verapamil. Systolic blood pressure in group 1 was significantly higher than that in groups 2 and 3 throughout the experiment. The pancreatic blood flow of the 11- week-old DS-S in group 2 was significantly greater than that in groups 1 and 3. Acinar degeneration with inflammatory changes and stromal fibrosis were observed in the pancreas of group 1 animals at 11 weeks of age, together with periarteritis nodosa. These pancreatic pathological findings were not observed in groups 2 and 3 at 11 weeks of age. TUNEL positive cells were not observed in the pancreas of 6-11 week DS-S in groups 1, 2 and 3. The process of apoptosis appears to have no effect on the pathology of pancreatic fibrosis in chronic ischemic pancreatitis. The body weight, systolic blood pressure and pancreatic blood flow of the 11-week-old DS-R did not significantly differ among the three groups. Pancreatic pathological findings were not observed in groups 4, 5 and 6 throughout the experiment, nor were TUNEL positive cells noted in the pancreas of 6-11 week DS-R in these groups. In conclusion, the pancreatic ischemia caused by stenosis of the arteries was an important factor in the pathogenesis of the pancreatitis in DS_S. (Accepted on December 18, 2001) Kawasaki Igakkaishi 28(1) : 11―21, 2002
