Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

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Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

Seiko Tanabe¹^,², Toshio Hata², and Masayasu Hiraoka¹

¹ Department of Cardiovascular Diseases, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510; and ² Department of Obstetrics and Gynecology, Saitama Medical School, Saitama 350-0451, Japan

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiologicaleffects of estrogen in isolated guinea pig ventricular myocytes.Action potentials and membrane currents were recorded using thewhole cell configuration of the patch-clamp technique. Applicationof 17 $beta$ -estradiol (10-30 µM) significantly prolonged the actionpotential duration (APD) at 20% (APD₂₀) and 90% repolarization(APD₉₀) at stimulation rates of 0.1-2.0 Hz. In the presence of30 µM 17 $beta$ -estradiol, APD₂₀ and APD₉₀ at 0.1 Hz were prolongedby 46.2 ± 17.1 and 63.4 ± 11.7% of the control (n = 5), respectively.In the presence of 30 µM 17 $beta$ -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 of30 µM 17 $beta$ -estradiol decreased the rapidly activating componentof 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 rectifierK⁺ current was barely affected. The results suggest that 17 $beta$ -estradiolprolonged APD mainly by inhibiting the I_K components I_Kr and I_Ks.

17 $beta$ -estradiol; Q-T interval; torsades de pointes; action potential duration; delayed outward potassium current

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