|
シガ ツヨシ
Tsuyoshi Shiga
志賀 剛 所属 医学部 医学科（東京女子医科大学病院） 職種 客員教授 |
|
| 論文種別 | 原著 |
| 言語種別 | 英語 |
| 査読の有無 | 査読あり |
| 表題 | Influence of beta-blockers on the myocardial mRNA expressions of circadian clock- and metabolism-related genes. |
| 掲載誌名 | 正式名：Journal of the American Society of Hypertension : JASH 略 称：J Am Soc Hypertens ISSNコード：18787436 |
| 掲載区分 | 国外 |
| 出版社 | Official Journal of the American Society of Hypertension |
| 巻・号・頁 | 7(2),pp.107-117 |
| 著者・共著者 | USHIJIMA Kentarou†, MAEKAWA Tomohiro, ISHIKAWA-KOBAYASHI Eiko, ANDO Hitoshi, SHIGA Tsuyoshi, FUJIMURA Akio |
| 発行年月 | 2013/03 |
| 概要 | Daily rhythms are regulated by a master clock-system in the suprachiasmatic nucleus and by a peripheral clock-system in each organ. Because norepinephrine is one of the timekeepers for the myocardial circadian clock that influences cardiac metabolism, it is speculated that a beta-blocker may affect the circadian clock and metabolism in heart tissue. In this study, thirty mg/kg/day of propranolol (a lipophilic beta-blocker) or atenolol (a hydrophilic beta-blocker) was given orally to Wistar rats for 4 weeks. The mRNA expressions of Bmal1 and E4BP4 in heart tissue were suppressed by the beta-blockers. However, the mRNA expressions of these clock genes in the suprachiasmatic nucleus were unchanged. Myocardial mRNA expressions of lactate dehydrogenase a and pyruvate dehydrogenase kinase 4 were also suppressed by the beta-blockers. In addition, ATP content in heart tissue was significantly elevated by the beta-blockers throughout 24 hours. The effects of propranolol and atenolol did not differ significantly. This study showed for the first time that a beta-blocker affects myocardial clock gene expression. Propranolol and atenolol increased ATP content in heart tissue throughout 24 hours. The influences of beta-blockers may be negligible on the SCN, and may be independent of lipid solubility on heart tissue. It is well known that these drugs exert a protective effect against myocardial ischemia, which may be mediated by an increase in the preservation of myocardial ATP. |
| DOI | 10.1016/j.jash.2012.12.007 |
| PMID | 23394803 |