File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Norepinephrine regulation of growth hormone release from goldfish pituitary cells. I. Involvement of α2 adrenoreceptor and interactions with dopamine and salmon gonadotropin-releasing hormone

TitleNorepinephrine regulation of growth hormone release from goldfish pituitary cells. I. Involvement of α2 adrenoreceptor and interactions with dopamine and salmon gonadotropin-releasing hormone
Authors
Issue Date2000
Citation
Journal Of Neuroendocrinology, 2000, v. 12 n. 4, p. 311-322 How to Cite?
AbstractAdrenergic regulation of growth hormone (GH) release in the goldfish was examined in vitro using dispersed goldfish pituitary cells under column perifusion. Norepinephrine and epinephrine suppressed basal GH release from goldfish pituitary cells in a reversible and dose-dependent manner. At high doses, a transient rebound of GH release was observed after termination of norepinephrine and epinephrine treatment. In this study, the dose-dependence of adrenergic inhibition on basal GH release was mimicked by the α2 agonists clonidine and UK14304. Basal GH secretion, however, was not affected by the β agonist isoproterenol and α1 agonist methoxamine. In addition, the inhibitory actions of norepinephrine and clonidine on basal GH release were blocked by the α2 antagonists yohimbine and RX821002. The β antagonist propranolol and α1 antagonists prasozin and benoxathian were not effective in this respect. Salmon gonadotropin-releasing hormone (sGnRH) and dopamine, two known GH-releasing factors in fish, stimulated GH release from goldfish pituitary cells and their GH-releasing actions were inhibited by simultaneous treatment with norepinephrine. Furthermore, the GH rebound after norepinephrine treatment was significantly enhanced by prior exposure to sGnRH and this effect was not observed with dopamine treatment. These results, taken together, suggest that in the goldfish adrenergic input at the pituitary level inhibit basal GH release through activation of α2 adrenoreceptors. This α2 inhibitory influence may interact with dopaminergic and GnRH input to regulate GH secretion from goldfish pituitary cells. The 'post-inhibition' GH rebound after NE treatment and its sensitivity to sGnRH potentiation may also represent a novel mechanism for GH regulation in fish.
Persistent Identifierhttp://hdl.handle.net/10722/178704
ISSN
2015 Impact Factor: 3.172
2015 SCImago Journal Rankings: 1.541
References

 

DC FieldValueLanguage
dc.contributor.authorLee, EKYen_US
dc.contributor.authorChan, VCCen_US
dc.contributor.authorChang, JPen_US
dc.contributor.authorYunker, WKen_US
dc.contributor.authorWong, AOLen_US
dc.date.accessioned2012-12-19T09:49:14Z-
dc.date.available2012-12-19T09:49:14Z-
dc.date.issued2000en_US
dc.identifier.citationJournal Of Neuroendocrinology, 2000, v. 12 n. 4, p. 311-322en_US
dc.identifier.issn0953-8194en_US
dc.identifier.urihttp://hdl.handle.net/10722/178704-
dc.description.abstractAdrenergic regulation of growth hormone (GH) release in the goldfish was examined in vitro using dispersed goldfish pituitary cells under column perifusion. Norepinephrine and epinephrine suppressed basal GH release from goldfish pituitary cells in a reversible and dose-dependent manner. At high doses, a transient rebound of GH release was observed after termination of norepinephrine and epinephrine treatment. In this study, the dose-dependence of adrenergic inhibition on basal GH release was mimicked by the α2 agonists clonidine and UK14304. Basal GH secretion, however, was not affected by the β agonist isoproterenol and α1 agonist methoxamine. In addition, the inhibitory actions of norepinephrine and clonidine on basal GH release were blocked by the α2 antagonists yohimbine and RX821002. The β antagonist propranolol and α1 antagonists prasozin and benoxathian were not effective in this respect. Salmon gonadotropin-releasing hormone (sGnRH) and dopamine, two known GH-releasing factors in fish, stimulated GH release from goldfish pituitary cells and their GH-releasing actions were inhibited by simultaneous treatment with norepinephrine. Furthermore, the GH rebound after norepinephrine treatment was significantly enhanced by prior exposure to sGnRH and this effect was not observed with dopamine treatment. These results, taken together, suggest that in the goldfish adrenergic input at the pituitary level inhibit basal GH release through activation of α2 adrenoreceptors. This α2 inhibitory influence may interact with dopaminergic and GnRH input to regulate GH secretion from goldfish pituitary cells. The 'post-inhibition' GH rebound after NE treatment and its sensitivity to sGnRH potentiation may also represent a novel mechanism for GH regulation in fish.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Neuroendocrinologyen_US
dc.rightsJournal of Neuroendocrinology. Copyright © Blackwell Publishing Ltd.-
dc.subject.meshAdrenergic Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDopamine - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGoldfishen_US
dc.subject.meshGonadotropin-Releasing Hormone - Physiologyen_US
dc.subject.meshGrowth Hormone - Secretionen_US
dc.subject.meshMaleen_US
dc.subject.meshNorepinephrine - Physiologyen_US
dc.subject.meshPituitary Gland - Cytology - Drug Effects - Secretionen_US
dc.subject.meshReceptors, Adrenergic, Alpha-2 - Physiologyen_US
dc.subject.meshSalmonen_US
dc.titleNorepinephrine regulation of growth hormone release from goldfish pituitary cells. I. Involvement of α2 adrenoreceptor and interactions with dopamine and salmon gonadotropin-releasing hormoneen_US
dc.typeArticleen_US
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_US
dc.identifier.authorityWong, AOL=rp00806en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2826.2000.00455.xen_US
dc.identifier.pmid10718928-
dc.identifier.scopuseid_2-s2.0-0034016991en_US
dc.identifier.hkuros53079-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034016991&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume12en_US
dc.identifier.issue4en_US
dc.identifier.spage311en_US
dc.identifier.epage322en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLee, EKY=7406968652en_US
dc.identifier.scopusauthoridChan, VCC=21736306800en_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridYunker, WK=24449778300en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats