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Article: Nongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epithelia

TitleNongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epithelia
Authors
Issue Date2001
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2001, v. 280 n. 5 49-5, p. C1160-C1167 How to Cite?
AbstractShort-circuit current (Isc) technique was used to investigate the role of testosterone in the regulation of chloride secretion in cultured rat efferent duct epithelia. Among the steroids tested, only testosterone, and to a lesser extent, 5α-dihydrotestosterone (5α-DHT), reduced the basal and forskolin-induced Isc in cultured rat efferent duct epithelia when added to the apical bathing solution. Indomethacin, a 3α-hydroxysteroid dehydrogenase, did not affect the inhibitory effect of 5α-DHT. The effect of testosterone occurred within 10-20 s upon application and was dose dependent with apparent IC50 value of 1 μM. The effect was abolished by removal of C1- but not HCO3 - from the normal Krebs-Henseleit solution, suggesting that testosterone mainly inhibited C1- secretion. The efferent duct was found to be most sensitive to testosterone, while the caput and the cauda epididymidis were only mildly sensitive. Cyproterone acetate, a steroidal antiandrogen, or flutamide, a nonsteroidal antiandrogen, did not block the effect of testosterone on the forskolin-induced Isc, nor did protein synthesis inhibitors, cycloheximide, or actinomycin D. However, pertussis toxin, a Gi protein inhibitor, attenuated the inhibition of forskolin-induced Isc by testosterone. Testosterone caused a dose-dependent inhibition of forskolin-induced rise in cAMP in efferent duct cells. It is suggested that the rapid effect of testosterone was mediated through a membrane receptor that is negatively coupled to adenylate cyclase via Gi protein. The role of nongenomic action of testosterone in the regulation of electrolyte and fluid transport in the efferent duct is discussed.
Persistent Identifierhttp://hdl.handle.net/10722/171264
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, GPHen_US
dc.contributor.authorChengChew, SBen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-10-30T06:13:03Z-
dc.date.available2012-10-30T06:13:03Z-
dc.date.issued2001en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2001, v. 280 n. 5 49-5, p. C1160-C1167en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/171264-
dc.description.abstractShort-circuit current (Isc) technique was used to investigate the role of testosterone in the regulation of chloride secretion in cultured rat efferent duct epithelia. Among the steroids tested, only testosterone, and to a lesser extent, 5α-dihydrotestosterone (5α-DHT), reduced the basal and forskolin-induced Isc in cultured rat efferent duct epithelia when added to the apical bathing solution. Indomethacin, a 3α-hydroxysteroid dehydrogenase, did not affect the inhibitory effect of 5α-DHT. The effect of testosterone occurred within 10-20 s upon application and was dose dependent with apparent IC50 value of 1 μM. The effect was abolished by removal of C1- but not HCO3 - from the normal Krebs-Henseleit solution, suggesting that testosterone mainly inhibited C1- secretion. The efferent duct was found to be most sensitive to testosterone, while the caput and the cauda epididymidis were only mildly sensitive. Cyproterone acetate, a steroidal antiandrogen, or flutamide, a nonsteroidal antiandrogen, did not block the effect of testosterone on the forskolin-induced Isc, nor did protein synthesis inhibitors, cycloheximide, or actinomycin D. However, pertussis toxin, a Gi protein inhibitor, attenuated the inhibition of forskolin-induced Isc by testosterone. Testosterone caused a dose-dependent inhibition of forskolin-induced rise in cAMP in efferent duct cells. It is suggested that the rapid effect of testosterone was mediated through a membrane receptor that is negatively coupled to adenylate cyclase via Gi protein. The role of nongenomic action of testosterone in the regulation of electrolyte and fluid transport in the efferent duct is discussed.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.mesh1-Methyl-3-Isobutylxanthine - Pharmacologyen_US
dc.subject.meshAcetazolamide - Pharmacologyen_US
dc.subject.meshAldosterone - Pharmacologyen_US
dc.subject.meshAmiloride - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnthranilic Acids - Pharmacologyen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshCell Membrane - Drug Effects - Physiologyen_US
dc.subject.meshChloride Channels - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshChlorides - Metabolismen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshDihydrotestosterone - Pharmacologyen_US
dc.subject.meshEpithelial Cells - Drug Effects - Physiologyen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshIon Channels - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMaleen_US
dc.subject.meshPhlorhizin - Pharmacologyen_US
dc.subject.meshProtein Synthesis Inhibitors - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshTestis - Cytology - Physiologyen_US
dc.subject.meshTestosterone - Pharmacologyen_US
dc.titleNongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epitheliaen_US
dc.typeArticleen_US
dc.identifier.emailLeung, GPH:gphleung@hkucc.hku.hken_US
dc.identifier.authorityLeung, GPH=rp00234en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11287329-
dc.identifier.scopuseid_2-s2.0-0035031478en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035031478&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume280en_US
dc.identifier.issue5 49-5en_US
dc.identifier.spageC1160en_US
dc.identifier.epageC1167en_US
dc.identifier.isiWOS:000168221100016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, GPH=35963668200en_US
dc.identifier.scopusauthoridChengChew, SB=6701358810en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US

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