scholarly journals Electrophysiological Effects of the Class Ic Antiarrhythmic Drug Pilsicainide on the Guinea-Pig Pulmonary Vein Myocardium

2012 ◽  
Vol 118 (4) ◽  
pp. 506-511 ◽  
Author(s):  
Akira Takahara ◽  
Kiyoshi Takeda ◽  
Yayoi Tsuneoka ◽  
Mihoko Hagiwara ◽  
Iyuki Namekata ◽  
...  
2013 ◽  
Vol 36 (2) ◽  
pp. 311-315 ◽  
Author(s):  
Akira Takahara ◽  
Kiyoshi Takeda ◽  
Mihoko Hagiwara ◽  
Hikaru Tanaka

2019 ◽  
Vol 141 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Masahiko Irie ◽  
Haruhito Hiiro ◽  
Shogo Hamaguchi ◽  
Iyuki Namekata ◽  
Hikaru Tanaka

1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.


1981 ◽  
Vol 15 (3) ◽  
pp. 131-136 ◽  
Author(s):  
H. REFSUM ◽  
J. P AMLIE ◽  
E. S PLATOU ◽  
T. OWREN ◽  
K. LANDMARK

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