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Conference Paper: The internal calcium store in airway muscle: Emptying, refilling and chloride. Possible new directions for drug development

TitleThe internal calcium store in airway muscle: Emptying, refilling and chloride. Possible new directions for drug development
Authors
Issue Date1992
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
Citation
The 5th Biochemical Pharmacology Symposium, Oxford, UK., 25-26 July 1991. In Biochemical Pharmacology, 1992, v. 43 n. 1, p. 29-37 How to Cite?
AbstractThis review examines the ionic mechanisms underlying acetylcholine (Ach) depolarization of airway smooth muscle and suggests that multiple mechanisms are involved. Increased chloride and non-specific cation conductance, and decreased or rapidly inactivating potassium conductances seem to be involved. Chloride ions also seem to play an important role in determining whether Ca2+ remains inside or is replenished in the sarcoplasmic reticulum (SR). The physiological role of Ach-induced depolarization is analysed and is suggested to be the promotion of the refilling of Ca2+ stores, partly through a direct refilling of SR-Ca2+ stores by way of an L-type Ca2+ channel. This refilling is promoted by Ca2+ channel agonists and is independent of the transmembrane potential. Ca2+-release by a variety of agonists leads to depolarization and stable membrane oscillations which depend on the action of the Ca2+-store uptake mechanisms in order to function. These oscillations may play a role in prolonged bronchoconstriction. Better knowledge of the control mechanisms of Ca(i)2+ is likely to reveal new targets for the therapy of asthma and provide a better understanding of the function of airway smooth muscle.
DescriptionConference Theme: Membrane Transport in Disease and Treatment
Persistent Identifierhttp://hdl.handle.net/10722/173437
ISSN
2015 Impact Factor: 5.091
2015 SCImago Journal Rankings: 2.263
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDaniel, EEen_US
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorAbela, Aen_US
dc.contributor.authorJury, Jen_US
dc.date.accessioned2012-10-30T06:31:24Z-
dc.date.available2012-10-30T06:31:24Z-
dc.date.issued1992en_US
dc.identifier.citationThe 5th Biochemical Pharmacology Symposium, Oxford, UK., 25-26 July 1991. In Biochemical Pharmacology, 1992, v. 43 n. 1, p. 29-37en_US
dc.identifier.issn0006-2952en_US
dc.identifier.urihttp://hdl.handle.net/10722/173437-
dc.descriptionConference Theme: Membrane Transport in Disease and Treatment-
dc.description.abstractThis review examines the ionic mechanisms underlying acetylcholine (Ach) depolarization of airway smooth muscle and suggests that multiple mechanisms are involved. Increased chloride and non-specific cation conductance, and decreased or rapidly inactivating potassium conductances seem to be involved. Chloride ions also seem to play an important role in determining whether Ca2+ remains inside or is replenished in the sarcoplasmic reticulum (SR). The physiological role of Ach-induced depolarization is analysed and is suggested to be the promotion of the refilling of Ca2+ stores, partly through a direct refilling of SR-Ca2+ stores by way of an L-type Ca2+ channel. This refilling is promoted by Ca2+ channel agonists and is independent of the transmembrane potential. Ca2+-release by a variety of agonists leads to depolarization and stable membrane oscillations which depend on the action of the Ca2+-store uptake mechanisms in order to function. These oscillations may play a role in prolonged bronchoconstriction. Better knowledge of the control mechanisms of Ca(i)2+ is likely to reveal new targets for the therapy of asthma and provide a better understanding of the function of airway smooth muscle.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharmen_US
dc.relation.ispartofBiochemical Pharmacologyen_US
dc.subject.meshAcetylcholine - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshChloride Channelsen_US
dc.subject.meshChlorides - Metabolismen_US
dc.subject.meshDrug Designen_US
dc.subject.meshMembrane Potentialsen_US
dc.subject.meshMembrane Proteins - Metabolismen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Metabolismen_US
dc.subject.meshNeuromuscular Depolarizing Agents - Pharmacologyen_US
dc.subject.meshRespiratory System - Metabolismen_US
dc.titleThe internal calcium store in airway muscle: Emptying, refilling and chloride. Possible new directions for drug developmenten_US
dc.typeConference_Paperen_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.doi10.1016/0006-2952(92)90657-5en_US
dc.identifier.pmid1310406-
dc.identifier.scopuseid_2-s2.0-0026544214en_US
dc.identifier.volume43en_US
dc.identifier.issue1en_US
dc.identifier.spage29en_US
dc.identifier.epage37en_US
dc.identifier.isiWOS:A1992HB64200007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDaniel, EE=35474017600en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridAbela, A=6602668587en_US
dc.identifier.scopusauthoridJury, J=7004287397en_US
dc.customcontrol.immutablesml 160602 amended-

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