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Adenylyl Cyclase Signaling in the Developing Chick Heart: The Deranging Effect of Antiarrhythmic Drugs
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SYSNO ASEP 0438496 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Adenylyl Cyclase Signaling in the Developing Chick Heart: The Deranging Effect of Antiarrhythmic Drugs Author(s) Hejnová, L. (CZ)
Hahnová, K. (CZ)
Kočková, Radka (FGU-C)
Svatůňková, Jarmila (FGU-C)
Sedmera, David (FGU-C) RID, ORCID, SAI
Novotný, J. (CZ)Source Title BioMed Research International. - : Hindawi - ISSN 2314-6133
Roč. 2014, č. 2014 (2014), s. 463123Number of pages 6 s. Language eng - English Country US - United States Keywords embryonic heart ; embryotoxicity ; adenylyl cyclase ; G protein ; beta-blocking agents Subject RIV FA - Cardiovascular Diseases incl. Cardiotharic Surgery R&D Projects GAP302/11/1308 GA ČR - Czech Science Foundation (CSF) Institutional support FGU-C - RVO:67985823 UT WOS 000338534700001 EID SCOPUS 84904158936 DOI 10.1155/2014/463123 Annotation The adenylyl cyclase (AC) signaling system plays a crucial role in the regulation of cardiac contractility. Here we analyzed the key components of myocardial AC signaling in the developing chick embryo and assessed the impact of selected beta-blocking agents on this system. Application of metoprolol and carvedilol, two commonly used beta-blockers, at embryonic day (ED) 8 significantly downregulated (by about 40%) expression levels of AC5, the dominant cardiac AC isoform, and the amount of Gs alpha protein at ED9. Activity of AC stimulated by forskolin was also significantly reduced under these conditions. Interestingly, when administered at ED4, these drugs did not produce such profound changes in the myocardial AC signaling system, except for markedly increased expression of Gi alpha protein. These data indicate that beta-blocking agents can strongly derange AC signaling during the first half of embryonic heart development Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2015
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