enalapril and Peptic-Ulcer

enalapril has been researched along with Peptic-Ulcer* in 2 studies

Trials

1 trial(s) available for enalapril and Peptic-Ulcer

Article	Year
[ACE inhibitors in the treatment of patients with arterial hypertension and pathology of the digestive system]. Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology, 2007, Issue:4 Topics: Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Enalapril; Fatty Liver; Female; Humans; Hypertension; Lisinopril; Liver Cirrhosis; Male; Middle Aged; Peptic Ulcer; Treatment Outcome	2007

Article

Year

[ACE inhibitors in the treatment of patients with arterial hypertension and pathology of the digestive system].

Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology, 2007, Issue:4

Topics: Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Enalapril; Fatty Liver; Female; Humans; Hypertension; Lisinopril; Liver Cirrhosis; Male; Middle Aged; Peptic Ulcer; Treatment Outcome

2007

Other Studies

1 other study(ies) available for enalapril and Peptic-Ulcer

Article	Year
Potassium channel modulators and indomethacin-induced gastric ulceration in rats. Scandinavian journal of gastroenterology, 1999, Volume: 34, Issue:10 Different mechanisms have been proposed for the pathophysiology of indomethacin-induced gastric ulceration (IIGU), including changes in gastric mucosal blood flow, motility, and acidity. It seems probable that adenosine 5'-triphosphate (ATP)-dependent potassium channels (K(ATP)) have a regulatory effect on the above factors. The aim of the present study was to investigate the effects of K(ATP) channel modulators, diazoxide as a channel opener and glibenclamide as a K(ATP) antagonist, on IIGU.. Male rats were starved for 24 h. Groups of 10 animals were used. Diazoxide at doses of 5, 15, and 45 mg/kg and glibenclamide at doses of 2, 6, and 18 mg/kg were injected intraperitoneally 30 min before the subcutaneous injection of 30 mg/kg of indomethacin. To assess the effects of indomethacin on the gastric mucosal vascular bed, different doses of enalapril and hydralazine, two vasodilators with mechanisms of action independent of K(ATP), were also studied. Gastric mucosal ulceration was noted, and fasting blood sugar was assayed. The data were compared between the groups.. Indomethacin produced gastric ulceration in 100% of rats with a severity rating of 2.15/10. This was prevented by diazoxide and aggravated by glibenclamide. Diazoxide increased and glibenclamide decreased fasting blood sugar. Neither enalapril nor hydralazine showed any effect on IIGU and/or fasting blood sugar.. K(ATP) modulators may play an important role in the pathophysiology of IIGU through a peripheral action on mucosal and submucosal blood flow of the stomach, gastric motility, acidity, or an action on the vagus complex center of the brain. Topics: Analysis of Variance; Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Glucose; Diazoxide; Enalapril; Gastric Mucosa; Glyburide; Hydralazine; Indomethacin; Male; Peptic Ulcer; Potassium Channel Blockers; Potassium Channels; Rats; Rats, Sprague-Dawley; Vasodilator Agents	1999

Article

Year

Potassium channel modulators and indomethacin-induced gastric ulceration in rats.

Scandinavian journal of gastroenterology, 1999, Volume: 34, Issue:10

Different mechanisms have been proposed for the pathophysiology of indomethacin-induced gastric ulceration (IIGU), including changes in gastric mucosal blood flow, motility, and acidity. It seems probable that adenosine 5'-triphosphate (ATP)-dependent potassium channels (K(ATP)) have a regulatory effect on the above factors. The aim of the present study was to investigate the effects of K(ATP) channel modulators, diazoxide as a channel opener and glibenclamide as a K(ATP) antagonist, on IIGU.. Male rats were starved for 24 h. Groups of 10 animals were used. Diazoxide at doses of 5, 15, and 45 mg/kg and glibenclamide at doses of 2, 6, and 18 mg/kg were injected intraperitoneally 30 min before the subcutaneous injection of 30 mg/kg of indomethacin. To assess the effects of indomethacin on the gastric mucosal vascular bed, different doses of enalapril and hydralazine, two vasodilators with mechanisms of action independent of K(ATP), were also studied. Gastric mucosal ulceration was noted, and fasting blood sugar was assayed. The data were compared between the groups.. Indomethacin produced gastric ulceration in 100% of rats with a severity rating of 2.15/10. This was prevented by diazoxide and aggravated by glibenclamide. Diazoxide increased and glibenclamide decreased fasting blood sugar. Neither enalapril nor hydralazine showed any effect on IIGU and/or fasting blood sugar.. K(ATP) modulators may play an important role in the pathophysiology of IIGU through a peripheral action on mucosal and submucosal blood flow of the stomach, gastric motility, acidity, or an action on the vagus complex center of the brain.

Topics: Analysis of Variance; Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Glucose; Diazoxide; Enalapril; Gastric Mucosa; Glyburide; Hydralazine; Indomethacin; Male; Peptic Ulcer; Potassium Channel Blockers; Potassium Channels; Rats; Rats, Sprague-Dawley; Vasodilator Agents

1999