File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Regulation of H1-receptor coupling and H1-receptor mRNA by histamine in bovine tracheal smooth muscle

TitleRegulation of H1-receptor coupling and H1-receptor mRNA by histamine in bovine tracheal smooth muscle
Authors
KeywordsAirway smooth muscle contraction
Desensitization
Gene expression
Histamine h1-receptor
Protein kinase C
Issue Date1998
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, 1998, v. 123 n. 5, p. 984-990 How to Cite?
Abstract1. Pretreatment of bovine tracheal smooth muscle (BTSM) with histamine (1-100 μM, 1 h) induced a concentration-dependent desensitization of the contractile response to subsequently administered histamine, with a reduction of the maximum response of 72 ± 8% (n = 5) following pre-exposure to 100 μM histamine. In contrast, concentration-response curves to the muscarinic agonist, methacholine were not affected following histamine pretreatment, indicating a homologous desensitization. Furthermore, concentration-response curves to NaF, a G-protein activator, were not altered following histamine pre-incubation. 2. The histamine H1-receptor (H1R) desensitization could be antagonized by mepyramine (an H1-receptor antagonist, 1 μM) but not by cimetidine (an H2-receptor antagonist, 10 μM), indicating that the desensitization occurred via stimulation of histamine H1-receptors. without evidence for the involvement of histamine H2-receptors. 3. Indomethacin (10 μM) did not block the H1R desensitization, suggesting no involvement of prostaglandins. Furthermore, histamine pre-incubation in calcium free medium still induced a functional uncoupling of H1R. 4. GF 109203X, a protein kinase C (PKC) inhibitor, and H-7, a non-selective kinase inhibitor, did not antagonize the homologous H1R desensitization. 5. The steady-state level of H1R mRNA, assessed by Northern blot analysis, was not affected by prolonged histamine exposure (100 μM. 0.5, 1, 2, 4, 16 and 24 h). 6. These results suggest that histamine induces desensitization of the H1R at the level of the receptor protein, which involves a mechanism independent of PKC, PKA, PKG and calcium influx suggesting the involvement of a receptor-specific kinase.
Persistent Identifierhttp://hdl.handle.net/10722/162217
ISSN
2023 Impact Factor: 6.8
2023 SCImago Journal Rankings: 2.119
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPype, JLen_US
dc.contributor.authorDupont, LJen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorBarnes, PJen_US
dc.contributor.authorVerleden, GMen_US
dc.date.accessioned2012-09-05T05:18:11Z-
dc.date.available2012-09-05T05:18:11Z-
dc.date.issued1998en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1998, v. 123 n. 5, p. 984-990en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/162217-
dc.description.abstract1. Pretreatment of bovine tracheal smooth muscle (BTSM) with histamine (1-100 μM, 1 h) induced a concentration-dependent desensitization of the contractile response to subsequently administered histamine, with a reduction of the maximum response of 72 ± 8% (n = 5) following pre-exposure to 100 μM histamine. In contrast, concentration-response curves to the muscarinic agonist, methacholine were not affected following histamine pretreatment, indicating a homologous desensitization. Furthermore, concentration-response curves to NaF, a G-protein activator, were not altered following histamine pre-incubation. 2. The histamine H1-receptor (H1R) desensitization could be antagonized by mepyramine (an H1-receptor antagonist, 1 μM) but not by cimetidine (an H2-receptor antagonist, 10 μM), indicating that the desensitization occurred via stimulation of histamine H1-receptors. without evidence for the involvement of histamine H2-receptors. 3. Indomethacin (10 μM) did not block the H1R desensitization, suggesting no involvement of prostaglandins. Furthermore, histamine pre-incubation in calcium free medium still induced a functional uncoupling of H1R. 4. GF 109203X, a protein kinase C (PKC) inhibitor, and H-7, a non-selective kinase inhibitor, did not antagonize the homologous H1R desensitization. 5. The steady-state level of H1R mRNA, assessed by Northern blot analysis, was not affected by prolonged histamine exposure (100 μM. 0.5, 1, 2, 4, 16 and 24 h). 6. These results suggest that histamine induces desensitization of the H1R at the level of the receptor protein, which involves a mechanism independent of PKC, PKA, PKG and calcium influx suggesting the involvement of a receptor-specific kinase.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.subjectAirway smooth muscle contraction-
dc.subjectDesensitization-
dc.subjectGene expression-
dc.subjectHistamine h1-receptor-
dc.subjectProtein kinase C-
dc.subject.mesh1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCattleen_US
dc.subject.meshCimetidine - Pharmacologyen_US
dc.subject.meshHistamine - Pharmacologyen_US
dc.subject.meshHistamine H1 Antagonists - Pharmacologyen_US
dc.subject.meshHistamine H2 Antagonists - Pharmacologyen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMaleimides - Pharmacologyen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Metabolismen_US
dc.subject.meshPyrilamine - Pharmacologyen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshReceptors, Histamine H1 - Genetics - Metabolismen_US
dc.subject.meshTrachea - Drug Effects - Metabolismen_US
dc.titleRegulation of H1-receptor coupling and H1-receptor mRNA by histamine in bovine tracheal smooth muscleen_US
dc.typeArticleen_US
dc.identifier.emailMak, JCW:judymak@hku.hken_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0701697en_US
dc.identifier.pmid9535029-
dc.identifier.scopuseid_2-s2.0-0031594724en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031594724&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume123en_US
dc.identifier.issue5en_US
dc.identifier.spage984en_US
dc.identifier.epage990en_US
dc.identifier.isiWOS:000072235600026-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridPype, JL=6602509935en_US
dc.identifier.scopusauthoridDupont, LJ=7102011073en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US
dc.identifier.scopusauthoridVerleden, GM=7006513432en_US
dc.identifier.issnl0007-1188-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats