{"title":"An attempt to characterize alpha-adrenoceptors on human dorsal foot veins in situ.","authors":"W Barthel","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effects of specific alpha-adrenergic agonists and antagonists on the congestion-induced change in the vessel diameter were studied in human dorsal foot veins in situ by means of a linear variable differential transformer. The specific agonist at alpha-1-adrenoceptors, phenylephrine, induced venoconstriction, whereas clonidine, the specific agonist at alpha-2-adrenoceptors, in this regard was ineffective, but on the contrary, lowered the phenylephrine-induced increase in venous tone. The phenylephrine-induced reaction could be inhibited in the rank order of their effectiveness by prazosin, the specific antagonist at alpha-1-adrenoceptors, by sodium nitroprusside and by verapamil. These results are in favour of the assumption that in exogenous stimulation of human foot veins by adrenergic agonists in situ, alpha-1-adrenoceptors are especially involved.</p>","PeriodicalId":13817,"journal":{"name":"International journal of clinical pharmacology, therapy, and toxicology","volume":"31 6","pages":"267-70"},"PeriodicalIF":0.0000,"publicationDate":"1993-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of clinical pharmacology, therapy, and toxicology","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 specific alpha-adrenergic agonists and antagonists on the congestion-induced change in the vessel diameter were studied in human dorsal foot veins in situ by means of a linear variable differential transformer. The specific agonist at alpha-1-adrenoceptors, phenylephrine, induced venoconstriction, whereas clonidine, the specific agonist at alpha-2-adrenoceptors, in this regard was ineffective, but on the contrary, lowered the phenylephrine-induced increase in venous tone. The phenylephrine-induced reaction could be inhibited in the rank order of their effectiveness by prazosin, the specific antagonist at alpha-1-adrenoceptors, by sodium nitroprusside and by verapamil. These results are in favour of the assumption that in exogenous stimulation of human foot veins by adrenergic agonists in situ, alpha-1-adrenoceptors are especially involved.