Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9534
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dc.contributor.authorDaly, Mark Jen
dc.contributor.authorOu, Ren
dc.contributor.authorGu, X Hen
dc.contributor.authorCasley, David Jen
dc.contributor.authorNayler, W Gen
dc.date.accessioned2015-05-15T22:39:45Z
dc.date.available2015-05-15T22:39:45Z
dc.date.issued1992-12-01en
dc.identifier.citationJournal of Molecular and Cellular Cardiology; 24(12): 1433-41en
dc.identifier.govdoc1293317en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9534en
dc.description.abstractThe binding characteristics of [125I]endothelin-1 (ET-1) to cardiac membranes isolated from rat hearts subjected to Ca(2+)-free perfusion or the Ca2+ paradox were examined. The effect of treatment with 2, 3 butanedione monoxime (BDM), which inhibits the tissue damage associated with the calcium paradox, was also investigated. Membranes from rat hearts perfused under control conditions bound [125I]ET-1 to a single population of sites with a Bmax of 107.7 +/- 3.7 fmol/mg protein and an affinity (KD) of 153 +/- 12 pM. Ten minutes of Ca(2+)-free perfusion resulted in a significant (P < 0.01) increase in Bmax to 167.5 +/- 8.3 fmol/mg protein without change in KD. Ca2+ repletion following Ca(2+)-free perfusion tended to increase further the Bmax (180.6 +/- 10.4 fmol/mg protein) without change in KD. Treatment with BDM attenuated but did not prevent the rise in Bmax following Ca(2+)-free perfusion. Following Ca2+ repletion, however, Bmax returned to control levels in the BDM treated group. These changes were not associated with changes in the ability of ET-1 and ET-3 to inhibit [125I]ET-1 binding. The results demonstrate that Ca(2+)-free perfusion is associated with an increase in the binding site density of [125I]ET-1 which is maintained or further increased upon Ca2+ repletion. If, however, the tissue damage associated with the Ca2+ paradox is prevented with BDM, Ca2+ repletion is associated with a reversal of the increase due to Ca(2+)-free perfusion.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBinding Sites.drug effects.physiologyen
dc.subject.otherCalcium.metabolism.physiologyen
dc.subject.otherDiacetyl.analogs & derivatives.pharmacologyen
dc.subject.otherEndothelins.metabolismen
dc.subject.otherFemaleen
dc.subject.otherHeart.drug effectsen
dc.subject.otherHomeostasis.drug effects.physiologyen
dc.subject.otherIodine Radioisotopes.diagnostic useen
dc.subject.otherMembrane Proteins.drug effects.metabolismen
dc.subject.otherMyocardium.metabolism.ultrastructureen
dc.subject.otherPerfusionen
dc.subject.otherProtein Bindingen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Endothelin.drug effects.metabolismen
dc.titleThe effects of Ca(2+)-free perfusion and the calcium paradox on [125I] endothelin-1 binding to rat cardiac membranes.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of molecular and cellular cardiologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages1433-41en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1293317en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
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