{"title":"Antiulcer activity of clonidine: lack of effect on gastric prostaglandins","authors":"Z. Ben-Zvi, V. Leibson","doi":"10.1016/0262-1746(87)90024-2","DOIUrl":null,"url":null,"abstract":"<div><p>Clonidine and paraaminoclonidine prevented the formation of indomethacin-induced gastric ulcers in female rats. This protective activity was blocked by coadministration of yohimbine. Therefore, the antiulcer activity of clonidine was due to its peripheral alpha-2 agonistic action. Because indomethacin is a prostaglandin synthetase inhibitor, its ulcerogenic effect has been attributed to a state of prostaglandin (PG) deficiency. We therefore investigated the possibility that the protective effect of alpha-2 adrenoceptor agonists could be mediated by stimulation of the biosynthesis of PGs in the stomach. However, the results failed to show incresed production of PGE<sub>2</sub> or 6-keto-PGF1, either in stomach slices <span><math><mtext>in vitro</mtext></math></span> or in the gastric mucosa of rats pretreated with clonidine, whether indomethacin was used or not. It is concluded that the activity of clonidine in preventing indomethacin-induced gastric erosions in rats is probably not related to prostaglandins.</p></div>","PeriodicalId":20720,"journal":{"name":"Prostaglandins, leukotrienes, and medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1987-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0262-1746(87)90024-2","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins, leukotrienes, and medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0262174687900242","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
Clonidine and paraaminoclonidine prevented the formation of indomethacin-induced gastric ulcers in female rats. This protective activity was blocked by coadministration of yohimbine. Therefore, the antiulcer activity of clonidine was due to its peripheral alpha-2 agonistic action. Because indomethacin is a prostaglandin synthetase inhibitor, its ulcerogenic effect has been attributed to a state of prostaglandin (PG) deficiency. We therefore investigated the possibility that the protective effect of alpha-2 adrenoceptor agonists could be mediated by stimulation of the biosynthesis of PGs in the stomach. However, the results failed to show incresed production of PGE2 or 6-keto-PGF1, either in stomach slices or in the gastric mucosa of rats pretreated with clonidine, whether indomethacin was used or not. It is concluded that the activity of clonidine in preventing indomethacin-induced gastric erosions in rats is probably not related to prostaglandins.
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