{"title":"Effects of angiotensin II on brain monoamine oxidase activity in non-hypoxic and hypoxic mice.","authors":"S Stancheva, V Georgiev, L Alova, D Getova","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effects of angiotensin II (ATII) administered intracerebroventricularly (i.c.v.) at a dose of 0.5 microgram per mouse on the activity of monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) in the forebrain of normoxic and hypoxic mice were studied. The influence of hypoxia (asphyctic and haemic) on MAO-A and MAO-B activity was also investigated. MAO-A activity was increased in haemic hypoxia; MAO-B activity increased in both asphyctic and haemic hypoxia. ATII increased MAO-A activity without affecting MAO-B activity under normoxic conditions. ATII increased MAO-A activity but decreased MAO-B in hypoxic (asphyctic) mice as compared to normoxic controls. The results suggest the role of MAO-A and MAO-B in the ATII-induced increase of susceptibility to acute hypoxia.</p>","PeriodicalId":7035,"journal":{"name":"Acta physiologica et pharmacologica Bulgarica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta physiologica et pharmacologica Bulgarica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The effects of angiotensin II (ATII) administered intracerebroventricularly (i.c.v.) at a dose of 0.5 microgram per mouse on the activity of monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) in the forebrain of normoxic and hypoxic mice were studied. The influence of hypoxia (asphyctic and haemic) on MAO-A and MAO-B activity was also investigated. MAO-A activity was increased in haemic hypoxia; MAO-B activity increased in both asphyctic and haemic hypoxia. ATII increased MAO-A activity without affecting MAO-B activity under normoxic conditions. ATII increased MAO-A activity but decreased MAO-B in hypoxic (asphyctic) mice as compared to normoxic controls. The results suggest the role of MAO-A and MAO-B in the ATII-induced increase of susceptibility to acute hypoxia.
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