Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10143
Full metadata record
DC FieldValueLanguage
dc.contributor.authorTanz, R Den
dc.contributor.authorNayler, W Gen
dc.date.accessioned2015-05-15T23:30:01Z
dc.date.available2015-05-15T23:30:01Z
dc.date.issued1991-07-08en
dc.identifier.citationArchives Internationales De Pharmacodynamie Et De The´rapie; 312(): 110-25en
dc.identifier.govdoc1663335en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10143en
dc.description.abstractAcetylcholine elicited an increase in developed tension on isolated porcine coronary arterial rings at concentrations exceeding 1.1 x 10(-7) M. However, at concentrations greater than 3.3 x 10(-6) M, desensitization occurred with repeated exposures to acetylcholine. When rings were first exposed to 3.3 x 10(-6) M, then washed and subsequently exposed to 3.3 x 10(-5) M, tension was either unchanged or significantly reduced, giving rise to two different population effects. Although atropine completely antagonized the effect of acetylcholine, pretreatment with methysergide (5-HT2), mepyramine (H1) and prazosin (alpha 1) did not attenuate acetylcholine-induced desensitization, indicating that the phenomenon is unrelated to either serotonin, H1- or alpha-adrenergic receptor activation. Diltiazem and nifedipine significantly reduced or completely inhibited contractions produced by K+ depolarization, but not those produced by acetylcholine. Moreover, ryanodine did not alter the tension developed by repeated exposures to acetylcholine. Our results suggest that acetylcholine activates specific receptor-operated channels which are less sensitive to calcium antagonists than K(+)-activated voltage-dependent channels. Moreover, acetylcholine-induced contractions in this model do not appear to be the result of calcium release from the sarcoplasmic reticulum since ryanodine failed to attenuate contractions.en
dc.language.isoenen
dc.subject.otherAcetylcholine.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherAtropine.pharmacologyen
dc.subject.otherCoronary Vessels.drug effectsen
dc.subject.otherDiltiazem.pharmacologyen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherMethysergide.pharmacologyen
dc.subject.otherMuscle Contraction.drug effectsen
dc.subject.otherMuscle Relaxation.drug effectsen
dc.subject.otherMuscle, Smooth, Vascular.drug effects.physiologyen
dc.subject.otherNifedipine.pharmacologyen
dc.subject.otherPotassium Chloride.pharmacologyen
dc.subject.otherPrazosin.pharmacologyen
dc.subject.otherPyrilamine.pharmacologyen
dc.subject.otherReceptors, Adrenergic, alpha.drug effectsen
dc.subject.otherSwineen
dc.titleConcentration-dependent desensitization of isolated porcine coronary arterial segments to acetylcholine.en
dc.typeJournal Articleen
dc.identifier.journaltitleArchives internationales de pharmacodynamie et de thérapieen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages110-25en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1663335en
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.cerifentitytypePublications-
Appears in Collections:Journal articles
Show simple item record

Page view(s)

6
checked on Feb 7, 2023

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.