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https://ahro.austin.org.au/austinjspui/handle/1/9534
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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Daly, Mark J | en |
dc.contributor.author | Ou, R | en |
dc.contributor.author | Gu, X H | en |
dc.contributor.author | Casley, David J | en |
dc.contributor.author | Nayler, W G | en |
dc.date.accessioned | 2015-05-15T22:39:45Z | |
dc.date.available | 2015-05-15T22:39:45Z | |
dc.date.issued | 1992-12-01 | en |
dc.identifier.citation | Journal of Molecular and Cellular Cardiology; 24(12): 1433-41 | en |
dc.identifier.govdoc | 1293317 | en |
dc.identifier.other | PUBMED | en |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/9534 | en |
dc.description.abstract | The 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.iso | en | en |
dc.subject.other | Animals | en |
dc.subject.other | Binding Sites.drug effects.physiology | en |
dc.subject.other | Calcium.metabolism.physiology | en |
dc.subject.other | Diacetyl.analogs & derivatives.pharmacology | en |
dc.subject.other | Endothelins.metabolism | en |
dc.subject.other | Female | en |
dc.subject.other | Heart.drug effects | en |
dc.subject.other | Homeostasis.drug effects.physiology | en |
dc.subject.other | Iodine Radioisotopes.diagnostic use | en |
dc.subject.other | Membrane Proteins.drug effects.metabolism | en |
dc.subject.other | Myocardium.metabolism.ultrastructure | en |
dc.subject.other | Perfusion | en |
dc.subject.other | Protein Binding | en |
dc.subject.other | Rats | en |
dc.subject.other | Rats, Sprague-Dawley | en |
dc.subject.other | Receptors, Endothelin.drug effects.metabolism | en |
dc.title | The effects of Ca(2+)-free perfusion and the calcium paradox on [125I] endothelin-1 binding to rat cardiac membranes. | en |
dc.type | Journal Article | en |
dc.identifier.journaltitle | Journal of molecular and cellular cardiology | en |
dc.identifier.affiliation | Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia | en |
dc.description.pages | 1433-41 | en |
dc.relation.url | https://pubmed.ncbi.nlm.nih.gov/1293317 | en |
dc.type.austin | Journal Article | en |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.grantfulltext | none | - |
item.languageiso639-1 | en | - |
item.openairetype | Journal Article | - |
Appears in Collections: | Journal articles |
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