作者: T. Brattelid , K. Tveit , J. A. K. Birkeland , I. Sjaastad , E. Qvigstad
DOI: 10.1007/S00395-007-0648-1
关键词:
摘要: Congestive heart failure (CHF) induces changes in the neurohumoral system and gene expression viable myocardium. Several of these genes encode G protein-coupled receptors (GPCRs) involved mechanisms which compensate for impaired myocardial function. We used real-time quantitative RT-PCR (Q-RT-PCR) to investigate mRNA encoding 15 different GPCRs possibly CHF, effect normalisation GAPDH (GAPDH) or 18S rRNA (18S). CHF was induced rats by coronary artery ligation, with sham-operated controls (Sham). After 6 weeks, left ventricular myocardium determined using both as standard. An apparent 30% reduction levels vs. compared Sham, although not significant itself, influenced interpretation regulation other genes.Thus, angiotensin II (AT1), endothelin (ETA, ETB) muscarinic acetylcholine (mACh) receptor M1 increased significantly only when normalised GAPDH. Levels mACh M3 M4 serotonin 5-HT2A 5-HT4 increased, whereas α1D-adrenoceptor decreased irrespective No change detected M2 M5 α1A-, α1B-, β1- β2-adrenoceptors. Q-RT-PCR is a sensitive powerful method monitor GPCR CHF. However, standard important regulation.