title: Thyroid hormone regulates mRNA expression and currents of ion channels in rat atrium.
abstract: Atrial fibrillation is one of the common arrhythmias associated with hyperthyroidism. This study examined the effects of thyroid hormone (T3) on mRNA expression and currents of major ionic channels determining the action potential duration (APD) in the rat atrium using the RNase protection assay and the whole-cell patch-clamp technique, respectively. T3 increased the Kv1.5 mRNA expression and decreased the L-type calcium channel mRNA expression, while the Kv4.2 mRNA expression did not change. APD was shorter in hyperthyroid than in euthyroid myocytes. The ultrarapid delayed rectifier potassium currents were remarkably increased in hyperthyroid than in euthyroid myocytes, whereas the transient outward potassium currents were unchanged. L-type calcium currents were decreased in hyperthyroid than in euthyroid myocytes. T3 shifted the current-voltage relationship for calcium currents negatively. In conclusion, T3 increased the outward currents and decreased the inward currents. The resultant changes of ionic currents shortened APD, providing a substrate for atrial fibrillation.
authors.affiliation: Division of Cardiology, Niigata University Graduate School of Medical and Dental Science, 1-754 Asahimachidori, Niigata, Japan. hiroshi7@med.niigata-u.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Meilei
authors.initials: M
authors.lastname: Ma
authors.forename: Takashi
authors.initials: T
authors.lastname: Washizuka
authors.forename: Satoru
authors.initials: S
authors.lastname: Komura
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Yukio
authors.initials: Y
authors.lastname: Hosaka
authors.forename: Katsuharu
authors.initials: K
authors.lastname: Hatada
authors.forename: Masaomi
authors.initials: M
authors.lastname: Chinushi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Kenichi
authors.initials: K
authors.lastname: Watanabe
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology; D016275:Atrial Function; D020746:Calcium Channels, L-Type / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D004553:Electric Conductivity; D005786:Gene Expression Regulation; D006325:Heart Atria / Q000378:metabolism; D006980:Hyperthyroidism / Q000150:complications; D007473:Ion Channels / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011917:Rats, Inbred Lew; D014284:Triiodothyronine / Q000494:pharmacology*
chemical_list: D020746:Calcium Channels, L-Type; D007473:Ion Channels; D015221:Potassium Channels; D012333:RNA, Messenger; D014284:Triiodothyronine