{"title":"Propranolol stereoselectively inhibits alpha-adrenoceptor-mediated vasoconstriction in mesenteric arterial beds of rats.","authors":"R E Stauber, A Heinemann","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>1. The optical isomers of propranolol were compared for their effects on pressor responses to adrenergic and non-adrenergic vasoconstrictors in mesenteric arterial beds of rats. 2. R(+)-propranolol (10(-7)-10(-5) M) had no effect on vessel preparations stimulated with noradrenaline, methoxamine, or arginine-vasopressin. 3. S(-)-propranolol 10(-7) M did not alter pressor responses to noradrenaline. However, S(-)-propranolol 10(-6) and 10(-5) M inhibited vasoconstriction induced by noradrenaline. This effect was similar in the presence of indomethacin 3 x 10(-6) M. 4. S(-)-propranolol 10(-5) M also inhibited vasoconstriction induced by methoxamine, shifting the dose-response curves to the right, but did not affect pressor responses to arginine-vasopressin. 5. Schild analysis for equilibrium vasoconstrictor responses to methoxamine indicated stereoselective competitive alpha-adrenoceptor antagonism by propranolol. 6. These data suggest selective inhibition of alpha-adrenoceptor-mediated vasoconstriction by S(-)-propranolol at higher concentrations by competitive alpha-adrenoceptor antagonism.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"125-9"},"PeriodicalIF":0.0000,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of autonomic pharmacology","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
1. The optical isomers of propranolol were compared for their effects on pressor responses to adrenergic and non-adrenergic vasoconstrictors in mesenteric arterial beds of rats. 2. R(+)-propranolol (10(-7)-10(-5) M) had no effect on vessel preparations stimulated with noradrenaline, methoxamine, or arginine-vasopressin. 3. S(-)-propranolol 10(-7) M did not alter pressor responses to noradrenaline. However, S(-)-propranolol 10(-6) and 10(-5) M inhibited vasoconstriction induced by noradrenaline. This effect was similar in the presence of indomethacin 3 x 10(-6) M. 4. S(-)-propranolol 10(-5) M also inhibited vasoconstriction induced by methoxamine, shifting the dose-response curves to the right, but did not affect pressor responses to arginine-vasopressin. 5. Schild analysis for equilibrium vasoconstrictor responses to methoxamine indicated stereoselective competitive alpha-adrenoceptor antagonism by propranolol. 6. These data suggest selective inhibition of alpha-adrenoceptor-mediated vasoconstriction by S(-)-propranolol at higher concentrations by competitive alpha-adrenoceptor antagonism.