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|Title:||The effects of Ca(2+)-free perfusion and the calcium paradox on [125I] endothelin-1 binding to rat cardiac membranes.|
|Authors:||Daly, Mark J;Ou, R;Gu, X H;Casley, David J;Nayler, W G|
|Affiliation:||Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Vic., Australia.|
|Citation:||Journal of Molecular and Cellular Cardiology; 24(12): 1433-41|
|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.|
|Internal ID Number:||1293317|
Binding Sites.drug effects.physiology
Diacetyl.analogs & derivatives.pharmacology
Iodine Radioisotopes.diagnostic use
Membrane Proteins.drug effects.metabolism
Receptors, Endothelin.drug effects.metabolism
|Appears in Collections:||Journal articles|
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