enalapril and Stomach-Ulcer

75% of patients systematically taking over the period of 6 weeks nonsteroidal anti-inflammatory drugs have their mucous of gastrointestinal tract pathologically changed. This process is called induced NSAID gastropathy. Inhibitors of angiotensin converting enzyme (I-ACE) seems to have gastroprotective effect by enhancing level of endogenous prostaglandins. Besides, an application of I-ACE reduces angiotensin II formation and activates renin-kallicrein-kinin system resulting in nitrogen oxide formation that is in its turn an important component of reparative process of mucous of gastrointestinal tract.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Captopril; Disease Models, Animal; Enalapril; Gastric Mucosa; Indomethacin; Lisinopril; Male; Rats; Stomach Ulcer; Treatment Outcome

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.

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Cholestasis; Enalapril; Male; Rats; Rats, Wistar; Stomach Ulcer; Stress, Physiological

To assess the mechanism of the effect of cigarette smoke on ulcer disease we employed a rat model in which cigarette smoke increases the size of acetic acid-induced gastric ulcer and decreases the hyperemia at the ulcer margin. We postulate that cigarette smoke increases angiotensin II (a vasoconstrictor) in ulcer tissue. Since direct measurement of angiotensin II in small tissue samples is problematic, we compared the messenger ribonucleic acid (mRNA) for its precursors (angiotensinogen and renin) in ulcer and normal gastric tissue. We also evaluated the effect of enalapril, which blocks the conversion of angiotensin I to angiotensin II on ulcer size. In the ulcer tissue, cigarette smoke produced a significant increase in mRNA for angiotensinogen but not for renin. Enalapril decreased the size of the gastric ulcer in rats exposed to cigarette smoke. The data support the possibility that in ulcer tissue cigarette smoke stimulates an angiotensin II-mediated mechanism, which may in part be responsible for the impairment of ulcer margin hyperemia and aggravation of ulcer size.

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Enalapril; Immunoblotting; Male; Platelet-Derived Growth Factor; Rats; Rats, Sprague-Dawley; Renin; RNA, Messenger; Smoking; Somatomedins; Stomach Ulcer; Transforming Growth Factor beta

We have compared the effect of the converting enzyme inhibitors, captopril and enalapril, on two models of gastric ulcers, viz; ethanol and oxyphenbutazone-induced lesions in rats. Both captopril and enalapril did not affect ethanol-induced lesions. While captopril significantly protected against oxyphenbutazone-induced lesions, enalapril aggravated the lesions. This difference is probably due to the lack of the protective sulfhydryl group in the chemical structure of enalapril.

Topics: Animals; Captopril; Enalapril; Ethanol; Male; Oxyphenbutazone; Rats; Rats, Inbred Strains; Stomach Ulcer