The pathogenetic role of endogenous angiotensin II in stress ulcer in obstructive jaundice rats

To investigate the pathogenetic role of endogenous angiotensin II (Ang II) in the mechanism of stress ulcer in obstructive jaundice rats and to detect the effect of angiotensin converting enzyme inhibitor (ACEI) on stress ulcer in obstructive jaundice rats.

After common bile duct ligation (CBDL) in Wistar rats, the content of plasma and gastric mucosal Ang II, gastric mucosal blood flow (GMBF) and gastric mucosal damage were measured, and the relationship among them was analyzed.

The plasma Ang II contents increased much more significantly at 1, 3, 7 and 14 days following CBDL than those in non-CBDL rats (P < 0.05, < 0.01, < 0.01 and < 0.01, respectively). Within 120 minutes following cold-restraint stress, plasma and gastric mucosal Ang II contents were elevated, GMBF decreased, and ulcer index and gastric mucosal damage increased more significantly than those in non-cold-restraint stress rats (P < 0.05, < 0.05, < 0.01, < 0.01 and < 0.05, respectively). Administration of an ACEI, enalaprili, to CBDL rats (5 mg.kg-1.day-1, orally for two days) before stress reduced both the plasma and gastric mucosal Ang II levels, inhibited the decrease of GMBF and decreased ulcer index and gastric mucosal damage (P < 0.001, < 0.01, < 0.01, < 0.01 and < 0.05, respectively).

The endogenous Ang II plays a significant pathogenetic role in the development of stress ulcer in obstructive jaundice rats, and ACEI may prevent stress ulcer.