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Article: Modulation of m2 receptors and excitation-contraction coupling in bovine airway smooth muscle

TitleModulation of m2 receptors and excitation-contraction coupling in bovine airway smooth muscle
Authors
Issue Date1996
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1996, v. 10 n. 3, p. A661 How to Cite?
AbstractIn airway smooth muscle, muscarinic stimulation is coupled to contraction independently of membrane potential. The consequence is that Ca++ channel blockers are ineffective in the treatment of airway diseases. Our earlier studies have shown that, following internal Ca++ stores depletion, coupling mechanism switches to membrane potential dependent and contraction is sensitive to voltage-dependent Ca++ channel blockers, in normal condition, M3 receptor stimulation is responsible for trachéal smooth muscle contraction while M2 receptors are silent. The aim of this study is to test whether switch in excitation-contraction coupling is due to modulation of M3 receptor to M3, following depletion of cyclopiazonic acid (CPA)- sensitive stores. In control medium, acetylcholine (ACh)-induced contraction was antagonized by 4DAMP (M3 antagonist) but not by gallamine (M2 antagonist). Following the depletion of the CPA sensitive stores, the potency of 4-DAMP decreased, while that of gallamine increased. Similarly, depletion of CPA sensitive stores and inhibition of M receptors, significantly increase the potency of cromakalim on AC h tonic contraction. Our results indicate that switch in excitation-contraction coupling observed following depletion of internal Ca++ stores only amplified M2 response and not modulation of M3 receptor.
Persistent Identifierhttp://hdl.handle.net/10722/171747
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorAmoako, DKen_US
dc.contributor.authorWan, CYKen_US
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:46Z-
dc.date.available2012-10-30T06:16:46Z-
dc.date.issued1996en_US
dc.identifier.citationFaseb Journal, 1996, v. 10 n. 3, p. A661en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/171747-
dc.description.abstractIn airway smooth muscle, muscarinic stimulation is coupled to contraction independently of membrane potential. The consequence is that Ca++ channel blockers are ineffective in the treatment of airway diseases. Our earlier studies have shown that, following internal Ca++ stores depletion, coupling mechanism switches to membrane potential dependent and contraction is sensitive to voltage-dependent Ca++ channel blockers, in normal condition, M3 receptor stimulation is responsible for trachéal smooth muscle contraction while M2 receptors are silent. The aim of this study is to test whether switch in excitation-contraction coupling is due to modulation of M3 receptor to M3, following depletion of cyclopiazonic acid (CPA)- sensitive stores. In control medium, acetylcholine (ACh)-induced contraction was antagonized by 4DAMP (M3 antagonist) but not by gallamine (M2 antagonist). Following the depletion of the CPA sensitive stores, the potency of 4-DAMP decreased, while that of gallamine increased. Similarly, depletion of CPA sensitive stores and inhibition of M receptors, significantly increase the potency of cromakalim on AC h tonic contraction. Our results indicate that switch in excitation-contraction coupling observed following depletion of internal Ca++ stores only amplified M2 response and not modulation of M3 receptor.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.titleModulation of m2 receptors and excitation-contraction coupling in bovine airway smooth muscleen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33749186225en_US
dc.identifier.volume10en_US
dc.identifier.issue3en_US
dc.identifier.spageA661en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridAmoako, DK=6506704096en_US
dc.identifier.scopusauthoridWan, CYK=36955231700en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US

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