Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9304
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dc.contributor.authorLouis, Simon N Sen
dc.contributor.authorJackman, G Pen
dc.contributor.authorNero, Tracy Len
dc.contributor.authorIakovidis, Den
dc.contributor.authorLouis, William Jen
dc.date.accessioned2015-05-15T22:21:12Z-
dc.date.available2015-05-15T22:21:12Z-
dc.date.issued2000-12-01en
dc.identifier.citationCardiovascular Drugs and Therapy / Sponsored By the International Society of Cardiovascular Pharmacotherapy; 14(6): 565-77en
dc.identifier.govdoc11300357en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9304en
dc.description.abstractIn vitro lipolysis stimulated by low (-)-isoprenaline concentrations (< or =30 nM) in epididymal white adipocytes from Sprague-Dawley rats was inhibited at least 60-80% by the specific beta1-antagonists LK 204-545 and CGP 20712A (1 microM), suggesting that at these low (10 nM) concentrations of (-)-isoprenaline lipolysis was primarily (80%) but not solely mediated via beta1-adrenergic receptors. Low concentrations (100 nM) of (-)-noradrenaline and formoterol also confirmed a role for beta1-adrenergic receptors in mediating lipolysis at low concentrations of these agonists. At higher agonist concentrations, beta3-adrenergic receptors were fully activated and were the dominant beta-adrenergic receptor subtype mediating the maximum lipolytic response, and the maximum response was not affected by the beta1-antagonists, demonstrating that the beta3-receptor is capable of inducing maximum lipolysis on its own. Studies of lipolysis induced by the relatively beta2-selective agonist formoterol in the presence of beta1-blockade (1 microM CGP 20712A) demonstrated the inability of the beta2-selective antagonist ICI 118-551 to inhibit the residual lipolysis at concentrations of ICI 118-551 < or = 1 microM. Higher concentrations of ICI 118-551 inhibited the residual formoterol-induced lipolysis competetively, but with low affinity (approximately 500-fold lower than its beta2-adrenergic receptor pA2, 7.80 +/- 0.21), suggesting that formoterol was not acting via beta2-adrenergic receptors. These data are consistent with beta1-adrenergic receptors playing an important role in lipolysis at physiological but not pharmacological concentrations of catecholamines and that beta2-adrenergic receptors play no obvious direct role in mediating beta-adrenergic receptor agonist-induced lipolysis in vitro. Finally, racemic-SR 59230A, unlike the pure (S, S)-isomer (a beta3-selective antagonist), was found to be a nonselective antagonist at the three beta-adrenergic receptor subtypes, showing that the other enantiomers have different selectivity.en
dc.language.isoenen
dc.subject.otherAdipocytes.drug effects.metabolismen
dc.subject.otherAdrenergic beta-Agonists.pharmacologyen
dc.subject.otherAdrenergic beta-Antagonists.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherFemaleen
dc.subject.otherHeart Rate.drug effectsen
dc.subject.otherIn Vitro Techniquesen
dc.subject.otherLipolysis.physiologyen
dc.subject.otherMaleen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Adrenergic, beta.physiologyen
dc.subject.otherReceptors, Adrenergic, beta-1.physiologyen
dc.subject.otherReceptors, Adrenergic, beta-2.physiologyen
dc.subject.otherReceptors, Adrenergic, beta-3.physiologyen
dc.titleRole of beta-adrenergic receptor subtypes in lipolysis.en
dc.typeJournal Articleen
dc.identifier.journaltitleCardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapyen
dc.identifier.affiliationUniversity of Melbourne, Clinical Pharmacology and Therapeutics Unit, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.description.pages565-77en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11300357en
dc.type.austinJournal Articleen
local.name.researcherLouis, William J
item.openairetypeJournal Article-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.grantfulltextnone-
crisitem.author.deptClinical Pharmacology and Therapeutics-
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