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dc.contributor.authorBergner, Albrecht
dc.contributor.authorSanderson, Michael J.
dc.date2022-08-11T08:10:03.000
dc.date.accessioned2022-08-23T16:53:29Z
dc.date.available2022-08-23T16:53:29Z
dc.date.issued2003-06-05
dc.date.submitted2008-08-04
dc.identifier.citationJ Appl Physiol. 2003 Sep;95(3):1325-32; discussion 1314. Epub 2003 May 30. <a href="http://dx.doi.org/10.1152/japplphysiol.00272.2003">Link to article on publisher's site</a>
dc.identifier.issn8750-7587 (Print)
dc.identifier.doi10.1152/japplphysiol.00272.2003
dc.identifier.pmid12777405
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42287
dc.description.abstractTo investigate the hypothesis that altered Ca2+ signaling in airway smooth muscle cells (SMCs) is responsible for airway hyperreactivity, we compared, with the use of confocal and phase-contrast microscopy, the airway contractility and Ca2+ changes in SMCs induced by acetylcholine (ACh) in lung slices from different mouse strains (A/J, Balb/C, and C3H/ HeJ). The airways from each mouse strain displayed a concentration-dependent contraction to ACh. The contractile response of the airways of the C3H/HeJ mice was found, in contrast to earlier studies, to be much greater and faster than that of A/J and Balb/C mice. This difference in airway reactivity can be, in part, attributable to halothane, a volatile anesthetic that was previously used during in vivo measurements of airway reactivity but found here to significantly alter the ACh contractile response of airways in lung slices. The ACh-induced Ca2+ response of the airway SMCs in all of the various mouse strains was also concentration dependent. The magnitude of the initial Ca2+ increase and the frequency of the subsequent Ca2+ oscillations induced by ACh increased with ACh concentration. However, no differences in the Ca2+ responses to ACh could be distinguished between the mouse strains. These results suggest that the mechanism responsible for airway hyperreactivity in different mouse strains resides with the Ca2+ sensitivity of the contractile apparatus of the SMCs rather than with the Ca2+ signaling itself.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12777405&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1152/japplphysiol.00272.2003
dc.subjectAcetylcholine
dc.subjectAnesthetics, Inhalation
dc.subjectAnimals
dc.subjectCalcium Signaling
dc.subjectCells, Cultured
dc.subjectHalothane
dc.subjectLung
dc.subjectMice
dc.subjectMice, Inbred A
dc.subjectMice, Inbred BALB C
dc.subjectMice, Inbred C3H
dc.subjectMicroscopy, Confocal
dc.subjectMuscle Contraction
dc.subjectMuscle, Smooth
dc.subjectSpecies Specificity
dc.subjectVasodilator Agents
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleAirway contractility and smooth muscle Ca(2+) signaling in lung slices from different mouse strains
dc.typeJournal Article
dc.source.journaltitleJournal of applied physiology (Bethesda, Md. : 1985)
dc.source.volume95
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/650
dc.identifier.contextkey564458
html.description.abstract<p>To investigate the hypothesis that altered Ca2+ signaling in airway smooth muscle cells (SMCs) is responsible for airway hyperreactivity, we compared, with the use of confocal and phase-contrast microscopy, the airway contractility and Ca2+ changes in SMCs induced by acetylcholine (ACh) in lung slices from different mouse strains (A/J, Balb/C, and C3H/ HeJ). The airways from each mouse strain displayed a concentration-dependent contraction to ACh. The contractile response of the airways of the C3H/HeJ mice was found, in contrast to earlier studies, to be much greater and faster than that of A/J and Balb/C mice. This difference in airway reactivity can be, in part, attributable to halothane, a volatile anesthetic that was previously used during in vivo measurements of airway reactivity but found here to significantly alter the ACh contractile response of airways in lung slices. The ACh-induced Ca2+ response of the airway SMCs in all of the various mouse strains was also concentration dependent. The magnitude of the initial Ca2+ increase and the frequency of the subsequent Ca2+ oscillations induced by ACh increased with ACh concentration. However, no differences in the Ca2+ responses to ACh could be distinguished between the mouse strains. These results suggest that the mechanism responsible for airway hyperreactivity in different mouse strains resides with the Ca2+ sensitivity of the contractile apparatus of the SMCs rather than with the Ca2+ signaling itself.</p>
dc.identifier.submissionpathoapubs/650
dc.contributor.departmentDepartment of Physiology
dc.source.pages1325-32; discussion 1314


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