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Decreased phosphodiesterase activities in cardiac hypertrophy

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dc.contributor.author Abi-Gerges, A. en_US
dc.contributor.author Castro, L.R.V. en_US
dc.contributor.author Leroy, J. en_US
dc.contributor.author Heymes, C. en_US
dc.contributor.author Samuel, J.-L. en_US
dc.contributor.author Lugnier, C. en_US
dc.contributor.author Fischmeister, R. en_US
dc.contributor.author Vandecasteele, G. en_US
dc.date.accessioned 2018-12-18T14:05:09Z
dc.date.available 2018-12-18T14:05:09Z
dc.date.copyright 2007 en_US
dc.identifier.issn 1095-8584 en_US
dc.identifier.uri http://hdl.handle.net/10725/9892
dc.description.abstract There is limited information on the changes in cardiac cyclic nucleotide phosphodiesterases (PDE1 to PDE5) during hypertrophy and the functional consequences on the cAMP pathway. To address this, 3-week-old rats were subjected to aortic stenosis (H) or sham operated (S). Hypertrophy was assessed at 8 weeks of age. Cyclic nucleotide-gated (CNG) channels were used to monitor cAMP. The whole cell patch-clamp technique was used to record the associated CNG current (ICNG) and ICa,L. Increased heart weight (43%) in the H group was accompanied by a general decrease in PDE activities in LV and a ≈ 50% reduction in PDE3 and PDE4. The efficacy of isoprenaline (Iso) to increase ICNG was decreased in H myocytes vs. S, whereas the response to forskolin (100 μM) was unchanged. The transient increase in ICa,L elicited by a 15 s application of Iso (100 nM) was similar in both groups. In S myocytes, PDE3 inhibition had no effect on ICa,L time-course, whereas PDE4 inhibition prolonged the signal. In H myocytes, both PDE3 or PDE4 inhibition slowed down ICa,L decay. Thus, PDE activities follow β1-AR desensitization in hypertrophy. Termination of β-AR stimulation of ICa,L is unchanged in hypertrophy, but the PDEs involved in this process are different. The contribution of PDE3 in hypertrophy might be seen as compensatory for the reduction in PDE4. en_US
dc.language.iso en en_US
dc.title Decreased phosphodiesterase activities in cardiac hypertrophy en_US
dc.type Article en_US
dc.description.version Published en_US
dc.title.subtitle Consequences for β-aR regulation of cAMP and ICa,L en_US
dc.author.school SOM en_US
dc.author.idnumber 201402416 en_US
dc.author.department N/A en_US
dc.description.embargo N/A en_US
dc.relation.journal Journal of Molecular and Cellular Cardiology en_US
dc.journal.volume 42 en_US
dc.journal.issue 6, Suppl. en_US
dc.article.pages S129 en_US
dc.keywords Hypertrophy en_US
dc.keywords L-type Ca2+ current en_US
dc.keywords Phosphodiesterases en_US
dc.identifier.doi https://doi.org/10.1016/j.yjmcc.2007.03.366 en_US
dc.identifier.ctation Abi-Gerges, A., Castro, L. R. V., Leroy, J., Heymes, C., Samuel, J. L., Lugnier, C., ... & Vandecasteele, G. (2007). Decreased phosphodiesterase activities in cardiac hypertrophy: Consequences for β-aR regulation of cAMP and ICa, L. Journal of Molecular and Cellular Cardiology, 42(6), S129. en_US
dc.author.email aniella.abigerges@lau.edu.lb en_US
dc.identifier.tou http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php en_US
dc.identifier.url https://www.sciencedirect.com/science/article/abs/pii/S0022282807004117 en_US
dc.orcid.id https://orcid.org/0000-0001-9974-4023 en_US
dc.author.affiliation Lebanese American University en_US


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