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Article: COX-dependent and -independent pathways in bradykinin-induced anion secretion in rat epididymis

TitleCOX-dependent and -independent pathways in bradykinin-induced anion secretion in rat epididymis
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 2002, v. 191 n. 2, p. 217-226 How to Cite?
AbstractLysylbradykinin (LBK) added to the apical or basolateral side of cultured rat epididymal monolayers stimulated a rise in short-circuit current (Isc) due to anion secretion. The concentration-response relationships for the apical and basolateral applications have EC 50 value of 0.001 μM. The responses to apical or basolateral application of LBK were blocked by WIN64338, a specific B 2 receptor antagonist, but not by Des-Arg 9,[Leu 8]-BK, a specific B 1 receptor antagonist, indicating that the LBK effects were mediated through B 2 bradykinin receptors. Experiments to desensitize the B 2 receptors by repeated stimulation have demonstrated that the responses to apical or basolateral LBK were due to discrete receptors on the apical or basolateral surface. In epithelia clamped in the Ussing chambers, addition of LBK to the apical or basolateral surface evoked release of PGE 2 into the apical and basolateral bathing solutions over the first 10 min following hormone addition. LBK added to the basolateral side elicited a greater release than it was added to the apical side. Pretreatment of the epithelia with piroxicam (5 μM) abolished PGE 2 release elicited by apical or basolateral LBK and abrogated the Isc induced by basolateral LBK. However, the rise in Isc induced by apical LBK was reduced by 31.3% only. The anion secretion response to apical LBK was not affected by MDL- 12330A, an adenylate cyclase inhibitor, but greatly attenuated by thapsigargin, an inhibitor of intracellular Ca 2+ release. However, the reverse effects were seen for basolateral LBK. It is concluded that distinct pathways are involved in the stimulation of anion secretion by apical or basolateral LBK. The response to basolateral LBK was COX-dependent, mediated by PGE 2 and involves cAMP as second messenger. In contrast, the response to apical LBK is largely COX-independent, not mediated by PGE 2 and involves Ca 2+ as intracellular messenger. © 2002 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/169745
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheuk, BLYen_US
dc.contributor.authorKo, WHen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-10-25T04:54:48Z-
dc.date.available2012-10-25T04:54:48Z-
dc.date.issued2002en_US
dc.identifier.citationJournal Of Cellular Physiology, 2002, v. 191 n. 2, p. 217-226en_US
dc.identifier.issn0021-9541en_US
dc.identifier.urihttp://hdl.handle.net/10722/169745-
dc.description.abstractLysylbradykinin (LBK) added to the apical or basolateral side of cultured rat epididymal monolayers stimulated a rise in short-circuit current (Isc) due to anion secretion. The concentration-response relationships for the apical and basolateral applications have EC 50 value of 0.001 μM. The responses to apical or basolateral application of LBK were blocked by WIN64338, a specific B 2 receptor antagonist, but not by Des-Arg 9,[Leu 8]-BK, a specific B 1 receptor antagonist, indicating that the LBK effects were mediated through B 2 bradykinin receptors. Experiments to desensitize the B 2 receptors by repeated stimulation have demonstrated that the responses to apical or basolateral LBK were due to discrete receptors on the apical or basolateral surface. In epithelia clamped in the Ussing chambers, addition of LBK to the apical or basolateral surface evoked release of PGE 2 into the apical and basolateral bathing solutions over the first 10 min following hormone addition. LBK added to the basolateral side elicited a greater release than it was added to the apical side. Pretreatment of the epithelia with piroxicam (5 μM) abolished PGE 2 release elicited by apical or basolateral LBK and abrogated the Isc induced by basolateral LBK. However, the rise in Isc induced by apical LBK was reduced by 31.3% only. The anion secretion response to apical LBK was not affected by MDL- 12330A, an adenylate cyclase inhibitor, but greatly attenuated by thapsigargin, an inhibitor of intracellular Ca 2+ release. However, the reverse effects were seen for basolateral LBK. It is concluded that distinct pathways are involved in the stimulation of anion secretion by apical or basolateral LBK. The response to basolateral LBK was COX-dependent, mediated by PGE 2 and involves cAMP as second messenger. In contrast, the response to apical LBK is largely COX-independent, not mediated by PGE 2 and involves Ca 2+ as intracellular messenger. © 2002 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_US
dc.relation.ispartofJournal of Cellular Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnions - Metabolismen_US
dc.subject.meshBradykinin - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Signaling - Drug Effects - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCyclooxygenase 1en_US
dc.subject.meshCyclooxygenase Inhibitors - Pharmacologyen_US
dc.subject.meshDinoprostone - Metabolism - Secretionen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEpididymis - Drug Effects - Enzymology - Secretionen_US
dc.subject.meshEpithelial Cells - Drug Effects - Enzymology - Secretionen_US
dc.subject.meshIon Channels - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshIsoenzymes - Drug Effects - Metabolismen_US
dc.subject.meshKallidin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshNaphthalenes - Pharmacologyen_US
dc.subject.meshOrganophosphorus Compounds - Pharmacologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Drug Effects - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Bradykinin - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleCOX-dependent and -independent pathways in bradykinin-induced anion secretion in rat epididymisen_US
dc.typeArticleen_US
dc.identifier.emailCheuk, BLY: bernice@hku.hken_US
dc.identifier.authorityCheuk, BLY=rp01671en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcp.10086en_US
dc.identifier.pmid12064465-
dc.identifier.scopuseid_2-s2.0-0036210814en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036210814&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume191en_US
dc.identifier.issue2en_US
dc.identifier.spage217en_US
dc.identifier.epage226en_US
dc.identifier.isiWOS:000174813600011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheuk, BLY=7801343617en_US
dc.identifier.scopusauthoridKo, WH=7202286822en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US

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