M. Samini, M. Mohagheghi, F. Hasanzadeh, A. Dehpour
{"title":"Anti‐ulcer Effect of Bromocriptine on Indomethacin‐induced Gastric Damage in Rats","authors":"M. Samini, M. Mohagheghi, F. Hasanzadeh, A. Dehpour","doi":"10.1211/146080800128736286","DOIUrl":null,"url":null,"abstract":"The anti-ulcer and gastroprotective effects of bromocriptine were studied in rats. Intraperitoneal administration of bromocriptine (2, 4 and 8 mg kg−1), a dopamine receptor agonist, which also acts on α-adrenoceptors, prevented indomethacin-induced gastric ulcer in rats dose-dependently. This protective effect was significantly blocked by the D1-receptor antagonist, SCH 23390 (1 mg kg−1, i.p.), the D2-receptor antagonist, sulpride (0.5 mg kg−1, i.p.) and the α2-receptor antagonist, yohimbine (5 mg kg−1, i.p.), suggesting that the effect of bromocriptine is mediated through dopamine receptors and α-adrenoceptors. \n \n \n \nWe propose that the anti-ulcer effect of bromocriptine may be due to a decrease in acid secretion and gastric motility through activation of α2-adrenoceptors and dopamine D1 receptors.","PeriodicalId":19946,"journal":{"name":"Pharmacy and Pharmacology Communications","volume":"9 1","pages":"411-413"},"PeriodicalIF":0.0000,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pharmacy and Pharmacology Communications","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1211/146080800128736286","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3
Abstract
The anti-ulcer and gastroprotective effects of bromocriptine were studied in rats. Intraperitoneal administration of bromocriptine (2, 4 and 8 mg kg−1), a dopamine receptor agonist, which also acts on α-adrenoceptors, prevented indomethacin-induced gastric ulcer in rats dose-dependently. This protective effect was significantly blocked by the D1-receptor antagonist, SCH 23390 (1 mg kg−1, i.p.), the D2-receptor antagonist, sulpride (0.5 mg kg−1, i.p.) and the α2-receptor antagonist, yohimbine (5 mg kg−1, i.p.), suggesting that the effect of bromocriptine is mediated through dopamine receptors and α-adrenoceptors.
We propose that the anti-ulcer effect of bromocriptine may be due to a decrease in acid secretion and gastric motility through activation of α2-adrenoceptors and dopamine D1 receptors.