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• W2044539742 abstract "In heart failure, chronic catecholaminergic stimulation increases diastolic Ca(2+) leak from ryanodine receptors (RyRs) of sarcoplasmic reticulum (SR), possibly due to the phosphorylation of RyRs through the activation of protein kinase A (PKA) or Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). In the present study, we attempted to identify which activated kinase is responsible for the enhanced Ca(2+) leak caused by beta-adrenergic stimulation. Trabeculae obtained from the hearts of adult male C57BL/6J mice were treated with isoproterenol and then permeabilized with saponin. To examine SR functions, Ca(2+) in SR was released with caffeine and measured with fluo-3. The Ca(2+) leak in isoproterenol-treated preparations was significantly increased when the PKA-dependent phosphorylation of RyR was increased without the involvement of CaMKII-dependent phosphorylation. Both the increase in Ca(2+) leak and the phosphorylation of RyR were blocked by a PKA inhibitor. Our results show that beta-adrenergic stimulation increases Ca(2+) leak from SR through PKA-dependent phosphorylation of RyR." @default.
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• W2044539742 date "2009-12-01" @default.
• W2044539742 modified "2023-10-15" @default.
• W2044539742 title "Protein kinase A-dependent phosphorylation of ryanodine receptors increases Ca2+ leak in mouse heart" @default.
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• W2044539742 doi "https://doi.org/10.1016/j.bbrc.2009.09.071" @default.
• W2044539742 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19781523" @default.
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