@article{oai:air.repo.nii.ac.jp:00002014,
 author = {Zhang, Chunpeng and Okamoto, Yosuke and Ohba, Takayoshi and Ishibashi, Kazuyuki and Yamamoto, Hiroshi and Ono, Kyoichi and Yamamoto, Fumio},
 issue = {2},
 journal = {秋田医学},
 month = {Feb},
 note = {Background : Cardiac hypertrophy is often associated with atrial arrhythmias, but there are limited experimental reports on small animal models of hypertrophied atria. Transverse aortic constriction (TAC) is an established model for ventricular hypertrophy and causes atrial hypertrophy and arrhythmias. Purpose : We aim to investigate the atrial remodeling caused by an experimental model of elevated afterload in rats. Methods and results : Eight weeks after creating TAC, hemodynamic, histological, and electrophysiological analyses were carried out in 8 week old rats. Sham operated rats were included as controls. The whole-cell patch-clamp technique was used to record action potentials (APs) and L-type Ca^<2+> current in isolated atrial myocytes. TAC resulted in hypertrophy in atrial and ventricular cardiomyocytes, accompanied by shortening of the atrial effective refractory period and an increase in atrial fibrillation (AF) inducibility by rapid atrial pacing. Atrial hypertrophy was associated with a shortening of AP duration and a decrease in L-type Ca^<2+> channel current density. Cav1.2 subunit mRNA expression was significantly reduced (p<0.05), which was paralleled by a significant increase in ANF and BNP expression in the TAC group compared with that in the sham group (p<0.05). Conclusions : TAC causes left atrial hypertrophy, associated with alteration of electrophysiological and molecular properties of L-type Ca^<2+> channels.},
 pages = {61--71},
 title = {DOWN-REGULATION OF L-TYPE CA2+ CURRENT IN LEFT ATRIAL MYOCYTES OF RATS DURING EXPERIMENTAL CARDIAC HYPERTROPHY},
 volume = {39},
 year = {2013}
}