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Article: Control of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscle

TitleControl of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscle
Authors
Issue Date2000
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/
Citation
American Journal Of Physiology - Lung Cellular And Molecular Physiology, 2000, v. 279 n. 4, p. L722-L732 How to Cite?
AbstractFull muscarinic stimulation in bovine tracheal smooth muscle caused a sustained contraction and increase in intracellular Ca2+ concentration ([Ca2+](i)) that was largely resistant to inhibition by nifedipine. Depletion of internal Ca2+ stores with cyclopiazonic acid resulted in an increased efficacy of nifedipine to inhibit this contraction and the associated increase in [Ca2+](i). Thus internal Ca2+ store depletion promoted electromechanical coupling between full muscarinic stimulation and muscle contraction to the detriment of pharmacomechanical coupling. A similar change in coupling mode was induced by ryanodine even when it did not significantly modify the initial transient increase in [Ca2+](i) induced by this stimulation, indicating that depletion of internal stores was not necessary to induce the change in excitation-contraction coupling mode. Blockade of the Ca2+-activated K+ channel by tetraethylammonium, charybdotoxin, and iberiotoxin all induced the change in excitation-contraction coupling mode. These results suggest that in this preparation, Ca2+ released from the ryanodine-sensitive Ca2+ store, by activating Ca2+-activated K+ channels, plays a central role in determining the expression of the pharmacomechanical coupling mode between muscarinic excitation and the Ca2+ influx necessary for the maintenance of tone.
Persistent Identifierhttp://hdl.handle.net/10722/171674
ISSN
2015 Impact Factor: 4.721
2015 SCImago Journal Rankings: 1.838
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTao, Len_US
dc.contributor.authorHuang, Yen_US
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:17Z-
dc.date.available2012-10-30T06:16:17Z-
dc.date.issued2000en_US
dc.identifier.citationAmerican Journal Of Physiology - Lung Cellular And Molecular Physiology, 2000, v. 279 n. 4, p. L722-L732en_US
dc.identifier.issn1040-0605en_US
dc.identifier.urihttp://hdl.handle.net/10722/171674-
dc.description.abstractFull muscarinic stimulation in bovine tracheal smooth muscle caused a sustained contraction and increase in intracellular Ca2+ concentration ([Ca2+](i)) that was largely resistant to inhibition by nifedipine. Depletion of internal Ca2+ stores with cyclopiazonic acid resulted in an increased efficacy of nifedipine to inhibit this contraction and the associated increase in [Ca2+](i). Thus internal Ca2+ store depletion promoted electromechanical coupling between full muscarinic stimulation and muscle contraction to the detriment of pharmacomechanical coupling. A similar change in coupling mode was induced by ryanodine even when it did not significantly modify the initial transient increase in [Ca2+](i) induced by this stimulation, indicating that depletion of internal stores was not necessary to induce the change in excitation-contraction coupling mode. Blockade of the Ca2+-activated K+ channel by tetraethylammonium, charybdotoxin, and iberiotoxin all induced the change in excitation-contraction coupling mode. These results suggest that in this preparation, Ca2+ released from the ryanodine-sensitive Ca2+ store, by activating Ca2+-activated K+ channels, plays a central role in determining the expression of the pharmacomechanical coupling mode between muscarinic excitation and the Ca2+ influx necessary for the maintenance of tone.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Lung Cellular and Molecular Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBethanechol - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshCattleen_US
dc.subject.meshCharybdotoxin - Pharmacologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMuscle Contraction - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Physiologyen_US
dc.subject.meshNifedipine - Pharmacologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshPotassium Channels - Drug Effects - Physiologyen_US
dc.subject.meshRyanodine - Pharmacologyen_US
dc.subject.meshTetraethylammonium - Pharmacologyen_US
dc.subject.meshTrachea - Drug Effects - Physiologyen_US
dc.titleControl of the mode of excitation-contraction coupling by Ca2+ stores in bovine trachealis muscleen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid11000133-
dc.identifier.scopuseid_2-s2.0-0033711376en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033711376&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume279en_US
dc.identifier.issue4en_US
dc.identifier.spageL722en_US
dc.identifier.epageL732en_US
dc.identifier.isiWOS:000089467300015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTao, L=14067858700en_US
dc.identifier.scopusauthoridHuang, Y=7501573013en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.customcontrol.immutablecsl 160524-

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