Changes in myocardial beta1-adrenergic receptor and stimulatory G-protein gene expression after chronic treatment with doxorubicin in rat

The gene expression of beta1-adrenergic receptor (beta1AR) and stimulatory G-protein Gsalpha in ventricle after chronic treatment with doxorubicin (DOX) in rat was investigated. The rats were treated with DOX in a dose of 2.5 mg/kg once a week for 5 weeks, the cumulative dose being 12.5 mg/kg. Two w...

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Veröffentlicht in:	Journal of veterinary medical science 2004-08, Vol.66 (8), p.989-992
Hauptverfasser:	Kizaki, K. (Kitasato Univ., Towada, Aomori (Japan). School of Veterinary Medicine and Animal Sciences), Akatsuka, K, Momozaki, M, Fujimori, Y, Uchide, T, Temma, K, Hara, Y
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Blotting, Northern Body Weight Cardiotonic Agents - metabolism Doxorubicin - pharmacology DRUGS GENE EXPRESSION Gene Expression Regulation - drug effects GTP-Binding Protein alpha Subunits, Gs - genetics GTP-Binding Protein alpha Subunits, Gs - metabolism Heart Ventricles - anatomy & histology Heart Ventricles - metabolism HORMONE RECEPTORS Isoproterenol - metabolism Models, Animal Organ Size RATS Receptors, Adrenergic, beta-1 - genetics Receptors, Adrenergic, beta-1 - metabolism RNA, Messenger - metabolism
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Zusammenfassung:	The gene expression of beta1-adrenergic receptor (beta1AR) and stimulatory G-protein Gsalpha in ventricle after chronic treatment with doxorubicin (DOX) in rat was investigated. The rats were treated with DOX in a dose of 2.5 mg/kg once a week for 5 weeks, the cumulative dose being 12.5 mg/kg. Two weeks after the last injection, the positive inotropic effect of isoproterenol was noticeably decreased in left atrial muscle preparations isolated from DOX-treated rats, Northern blot hybridization showed that die mRNA transcripts of beta1AR and Gsalpha, important signal transduction elements for regulating heart rate and contractility, were significantly decreased in the ventricle of DOX-treated rats. Thus, chronic treatment with DOX decreases the gene expression levels of myocardial beta1AR and Gsalpha.
ISSN:	0916-7250 1347-7439
DOI:	10.1292/jvms.66.989