Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9341
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dc.contributor.authorFabiani, Mark Een
dc.contributor.authorSourial, Men
dc.contributor.authorThomas, W Gen
dc.contributor.authorJohnston, Colin Ien
dc.contributor.authorFrauman, Albert Gen
dc.date.accessioned2015-05-15T22:24:10Z
dc.date.available2015-05-15T22:24:10Z
dc.date.issued2001-10-01en
dc.identifier.citationThe Journal of Endocrinology; 171(1): 97-108en
dc.identifier.govdoc11572794en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9341en
dc.description.abstractThe renin-angiotensin system (RAS) is present in the human prostate and may be activated in benign prostatic hyperplasia (BPH), possibly contributing to the pathophysiology of this disorder by enhancing local sympathetic tone and cell growth. The functional role of the RAS in the prostate, however, is unknown. The present study was undertaken to determine whether angiotensin (Ang) II enhances sympathetic transmission in the prostate. The neuronal stores of the rat prostate were labelled with [(3)H]noradrenaline (NA). Ang II and Ang I enhanced [(3)H]NA release in a concentration-dependent manner. The Ang II receptor subtype 1 (AT(1) receptor) antagonist losartan and the AT(2) receptor antagonist PD123319 inhibited this facilitatory effect of Ang II and Ang I, whereas the other AT(2) receptor antagonist, CGP42112, was without effect. Bradykinin also increased [(3)H]NA release, which was inhibited by the B(2) receptor antagonist Hoe140. The angiotensin-converting enzyme inhibitor captopril inhibited the effect of Ang I, but potentiated that of bradykinin. Interestingly, captopril alone produced an increase in [(3)H]NA release which was inhibited by Hoe140. Losartan, but not PD123319 or CGP42112, inhibited [(125)I]-Ang II binding in Chinese hamster ovary cells transfected with the AT(1a) or AT(1b) receptor. In contrast, in cells expressing the AT(2) receptor, PD123319 and CGP42112, but not losartan, inhibited [(125)I]-Ang II binding. In conclusion, Ang II enhances the release of NA from sympathetic nerves of the rat prostate via a novel functional receptor distinct from the cloned AT(1a), AT(1b) or AT(2). These data provide direct evidence in support of a functional role for the local RAS in modulating sympathetic transmission in the prostate, which may have important implications for the pathophysiology of BPH.en
dc.language.isoenen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAngiotensin I.pharmacologyen
dc.subject.otherAngiotensin II.pharmacologyen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherBradykinin.analogs & derivatives.pharmacologyen
dc.subject.otherCHO Cells.drug effectsen
dc.subject.otherCaptopril.pharmacologyen
dc.subject.otherCricetinaeen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherImidazoles.pharmacologyen
dc.subject.otherLosartan.pharmacologyen
dc.subject.otherMaleen
dc.subject.otherNorepinephrine.secretionen
dc.subject.otherOligopeptides.pharmacologyen
dc.subject.otherProstate.innervationen
dc.subject.otherProstatic Hyperplasia.physiopathologyen
dc.subject.otherPyridines.pharmacologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Angiotensin.metabolismen
dc.subject.otherSympathetic Nervous System.drug effects.secretionen
dc.subject.otherSynaptic Transmission.drug effectsen
dc.titleAngiotensin II enhances noradrenaline release from sympathetic nerves of the rat prostate via a novel angiotensin receptor: implications for the pathophysiology of benign prostatic hyperplasia.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of Endocrinologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg VIC 3084, Australiaen
dc.description.pages97-108en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11572794en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptClinical Pharmacology and Therapeutics-
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