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Article: Characterization of adrenoceptors involved in the electrogenic chloride secretion by cultured rat epididymal epithelium

TitleCharacterization of adrenoceptors involved in the electrogenic chloride secretion by cultured rat epididymal epithelium
Authors
Issue Date1992
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1992, v. 107 n. 1, p. 146-151 How to Cite?
Abstract1. Short-circuit current (SCC) technique was used to study the adrenoceptors involved in the electrogenic chloride secretion by cultured cauda epididymal epithelium of rats. Stimulation of the epithelium with noradrenaline (primarily β 1-adrenoceptor selective agonist), salbutamol (β 2-adrenoceptor selective agonist) and adrenaline (non-selective β-adrenoceptor agonist) led to a rise in SCC. At a low chart-speed (2 mm min -1), the response profile to these agonists consisted of a peak followed by a sustained response considerably higher than the basal SCC. 2. The EC 50s (doses of agonist producing 50% maximum response) of noradrenaline, salbutamol and adrenaline were 300, 115 and 10 nM respectively. Pretreating the tissues with 1 μM atenolol (β 1-selective antagonist) and 10 μM butoxamine (β 2-selective antagonist) shifted the dose-response curves of noradrenaline (shifted EC 50 = 4000 nM) and salbutamol (shifted EC 50 = 1050 nM) to the right. Atenolol (1 μM) and butoxamine (10 μM) shifted the dose-response curve of adrenaline to the right with new EC 50s of 30 nM and 115 nM, respectively. 3. The rapidly rising phase of the SCC response to noradrenaline and adrenaline observed at low chart-speed consisted of a brief and transient retraction followed by a rebound increase in SCC. At a high chart-speed (1 mm s -1), the retraction and rebound phenomenon manifested as a fast initial spike which could be blocked by phentolamine (non-specific α-adrenoceptor antagonist) in a dose-dependent fashion. Similar initial spikes were observed when the tissues were stimulated with phenylephrine (α 1-selective agonist) but not with isoprenaline (non-selective β-agonist) or forskolin (activator of adenylate cyclase). The response of the initial spike triggered by noradrenaline was dose-dependent and the EC 50 was 2000 nM. 4. The present study showed that the electrogenic chloride secretion by rat epididymis could be stimulated by α 1-, β 1- and β 2-adrenoceptor agonists. The α 1-mediated response had a faster onset and more transient action than the β-counterpart. It is postulated that epididymal chloride secretion might be regulated by neural (noradrenaline-mediated) and humoral (adrenaline-mediated) controls and that the stimulus-secretion coupling mechanisms might involve both Ca 2+ (α 1-mediated response) and adenosine 3':5'-cyclic monophosphate (β-mediated response) as intracellular second messengers.
Persistent Identifierhttp://hdl.handle.net/10722/161943
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLeung, AYHen_US
dc.contributor.authorYip, WKen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-09-05T05:16:12Z-
dc.date.available2012-09-05T05:16:12Z-
dc.date.issued1992en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1992, v. 107 n. 1, p. 146-151en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/161943-
dc.description.abstract1. Short-circuit current (SCC) technique was used to study the adrenoceptors involved in the electrogenic chloride secretion by cultured cauda epididymal epithelium of rats. Stimulation of the epithelium with noradrenaline (primarily β 1-adrenoceptor selective agonist), salbutamol (β 2-adrenoceptor selective agonist) and adrenaline (non-selective β-adrenoceptor agonist) led to a rise in SCC. At a low chart-speed (2 mm min -1), the response profile to these agonists consisted of a peak followed by a sustained response considerably higher than the basal SCC. 2. The EC 50s (doses of agonist producing 50% maximum response) of noradrenaline, salbutamol and adrenaline were 300, 115 and 10 nM respectively. Pretreating the tissues with 1 μM atenolol (β 1-selective antagonist) and 10 μM butoxamine (β 2-selective antagonist) shifted the dose-response curves of noradrenaline (shifted EC 50 = 4000 nM) and salbutamol (shifted EC 50 = 1050 nM) to the right. Atenolol (1 μM) and butoxamine (10 μM) shifted the dose-response curve of adrenaline to the right with new EC 50s of 30 nM and 115 nM, respectively. 3. The rapidly rising phase of the SCC response to noradrenaline and adrenaline observed at low chart-speed consisted of a brief and transient retraction followed by a rebound increase in SCC. At a high chart-speed (1 mm s -1), the retraction and rebound phenomenon manifested as a fast initial spike which could be blocked by phentolamine (non-specific α-adrenoceptor antagonist) in a dose-dependent fashion. Similar initial spikes were observed when the tissues were stimulated with phenylephrine (α 1-selective agonist) but not with isoprenaline (non-selective β-agonist) or forskolin (activator of adenylate cyclase). The response of the initial spike triggered by noradrenaline was dose-dependent and the EC 50 was 2000 nM. 4. The present study showed that the electrogenic chloride secretion by rat epididymis could be stimulated by α 1-, β 1- and β 2-adrenoceptor agonists. The α 1-mediated response had a faster onset and more transient action than the β-counterpart. It is postulated that epididymal chloride secretion might be regulated by neural (noradrenaline-mediated) and humoral (adrenaline-mediated) controls and that the stimulus-secretion coupling mechanisms might involve both Ca 2+ (α 1-mediated response) and adenosine 3':5'-cyclic monophosphate (β-mediated response) as intracellular second messengers.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChlorides - Metabolismen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshEpididymis - Drug Effects - Metabolismen_US
dc.subject.meshEpithelium - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Physiologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Physiologyen_US
dc.titleCharacterization of adrenoceptors involved in the electrogenic chloride secretion by cultured rat epididymal epitheliumen_US
dc.typeArticleen_US
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_US
dc.identifier.authorityLeung, AYH=rp00265en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1476-5381.1992.tb14477.x-
dc.identifier.pmid1358380-
dc.identifier.scopuseid_2-s2.0-0026715099en_US
dc.identifier.volume107en_US
dc.identifier.issue1en_US
dc.identifier.spage146en_US
dc.identifier.epage151en_US
dc.identifier.isiWOS:A1992JK06700024-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLeung, AYH=7403012668en_US
dc.identifier.scopusauthoridYip, WK=35836563800en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US

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