抄録
To investigate whether thyroid hormone modulates electrical properties of atrial myocytes, electrocardiogram (ECG), action potentials (APs), and ionic currents were measured. Male Sprague-Dawley rats were randomly divided into control and T4-treated groups at 6 weeks of age. L-thyroxine (500 μg/kg body weight) was daily injected into peritoneal cavity for 14 days (T4-treated rats) and the same volume of saline was daily injected in control rats. ECG signals were recorded using apex-base lead. APs, voltage-dependent Na+ and L-type Ca2+ channel current (INa and ICa(L)), inwardly rectifying K+ channel current (IK1), transient outward K+ channel current (Ito), and delayed rectifier K+ channel current (IK(delay)) were measured using patch-clamp techniques. T4-treatment significantly changed electrical properties in rat atrial myocytes including the increase in cell membrane capacitance, the decrease in input resistance, and the shortening of AP duration. ECG revealed sinus tachycardia in T4-treated rats. Voltage-clamp recording revealed the current densities of INa and IK1 in T4-treated atrial myocytes did not differ from those in control cells. However, the current density of ICa(L) was significantly decreased and the current density IK(delay) was significantly increased in T4-treated rats. Thus, thyrotoxicosis could induce the shortening of AP duration by alterations in the current densities of both ICa(L) and IK(delay) in rat atrial myocytes. [Jpn J Physiol 54 Suppl:S104 (2004)]
