Molecular and Electrical Remodeling of L- and T-Type Ca2+ Channels in Rat Right Atrium With Monocrotaline-Induced Pulmonary Hypertension

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Background Atrial arrhythmia is often encountered in chronic pulmonary disease with pulmonary hypertension (PH), but few studies have investigated the electrical remodeling of atrial Ca2+ channels under PH. Methods and Results Wistar rats were injected with monocrotaline (MCT), resulting in PH with right atrial and ventricular hypertrophy. The L-type Ca2+ channel current density was significantly decreased in right atrial cells of MCT-treated rats, accompanied by a significant reduction in mRNA expression of the CaV1.2 (α1C) subunit and accessory β2 subunit. Conversely, the low voltage-activated Ca2+ current was more marked in the right atrial cells of MCT-treated rats than in those of control rats. The current-voltage relationship and the time course of inactivation closely resembled those of T-type Ca2+ channels, although the current was only slightly inhibited by 10-100 μmol/L Ni2+. No significant differences were observed in the mRNA expression levels of CaV3.1 (α1G) and CaV3.2 (α1H) or the protein level of the CaV3.1 subunit. In left atrial cells, the electrophysiological molecular properties of Ca2+ channels were unaffected by MCT treatment. Conclusions PH causes right atrial hypertrophy, associated with alteration of the electrophysiological molecular properties of Ca2+ channels.