title: Presence and functional role of the rapidly activating delayed rectifier K(+) current in left and right atria of adult mice.
abstract: Repolarization of cardiac action potentials is regulated by several types of K(+) currents. The present study examined the presence and functional significance of rapid delayed rectifier (I(Kr)) in left and right atrial myocytes of mouse heart, using whole-cell patch-clamp method. The functional role of ultrarapid delayed rectifier (I(Kur)) in the repolarization was also examined by blocking with 4-aminopyridine (50 μM). The presence of I(Kr) was detected in left and right atrial myocytes as an E-4031 (5 μM)-sensitive current that exhibited relatively rapid activation during depolarization and half activation voltage of -17.5 and -17.4 mV for left and right atrial myocytes, respectively. The current density of I(Kr) was similar between left and right atria. The prolongation of action potential measured at 50% repolarization evoked by 4-aminopyridine was significantly larger in left than in right atrium, which appears to be consistent with the larger amplitude of I(Kur) in left atrium. On the other hand, the prolongation of action potential measured at 90% repolarization caused by E-4031 was significantly larger in right than in left atrium. The longer action potential of right atrium, which may result at least partly from smaller amplitude of I(Kur), is likely to enhance the functional significance of I(Kr) in repolarization process of right atrium, despite of similar magnitude of I(Kr) in left and right atria. Our data thus identifies I(Kr) in mouse atria and indicates the presence of functional interaction between I(Kr) and I(Kur) that potentially contributes to repolarization heterogeneity in left and right atria of mouse heart.
authors.affiliation: Division of Neurology, Department of Internal Medicine, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
authors.forename: Hiroko
authors.initials: H
authors.lastname: Nakamura
authors.forename: Wei-Guang
authors.initials: WG
authors.lastname: Ding
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Sanada
authors.forename: Kengo
authors.initials: K
authors.lastname: Maeda
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Kawai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Maegawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Matsuura
mesh_terms: D000200:Action Potentials / Q000187:drug effects*; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D016275:Atrial Function / Q000187:drug effects*; D002478:Cells, Cultured; D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels / Q000037:antagonists & inhibitors / Q000502:physiology*; D006325:Heart Atria / Q000166:cytology / Q000187:drug effects; D007700:Kinetics; D051666:Kv1.5 Potassium Channel / Q000037:antagonists & inhibitors / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000502:physiology; D009928:Organ Specificity; D018408:Patch-Clamp Techniques; D010880:Piperidines / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology
chemical_list: D000631:Aminopyridines; D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; C496982:Kcna5 protein, mouse; D051666:Kv1.5 Potassium Channel; D010880:Piperidines; D026902:Potassium Channel Blockers; D011725:Pyridines; C063968:E 4031; C084482:4-aminopyridine methiodide