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These results suggest that the preferential reduction in the density of Ito in the CT cells could contribute to prolong their APD, which may be related to the genesis of atrial reentry.

1 The eects of oestrogens on action potential and membrane currents were examined in single guinea-pig atrial myocytes. 2 17b-estradiol (3 ± 10 mM) shortened the action potential duration without signi®cant changes in the resting membrane potential. E-4031 (1 mM) markedly prolonged the action potential duration and induced early afterdepolarization, and 17b-estradiol (10 mM) abolished it. 3 When cells were perfused in isoproterenol-containing solution, action potentials due to abnormal automaticity caused by membrane depolarization developed, and were also inhibited by 17b-estradiol. 4 Under voltage clamp conditions, the voltage-dependent Ca 2+ currents consisted of both T-(I Ca.T ) and L-type (I Ca.L ). 17b-estradiol reduced I Ca.L concentration-dependently, while it (10 mM) suppressed I Ca.T only by approximately 10%. 17b-estradiol did not aect time courses of I Ca.L inactivation, but it shifted the steady-state inactivation curve to more negative potentials. 5 17b-estradiol (10 mM) did not aect the time-dependent K + current (I K ), referred to as I Kr and I Ks , and inwardly rectifying K + current. However, 17b-estradiol (30 mM) or diethylstilbestrol (10 mM) inhibited K + currents. 6 DES and ethinylestradiol (EES) also suppressed I Ca.L , but testosterone and progesterone failed to inhibit I Ca.L . The potency of the inhibitory eect on I Ca.L was DES4EES417b-estradiol. 7 17b-estradiol and DES also inhibited the cyclic AMP-enhanced I Ca.L , but cyclic GMP in the pipette or pretreatment of L-NAME could not block the eects of oestrogen on I Ca.L . 8 These results suggest that oestrogen speci®cally has antiarrhythmic eects, possibly by acting the L-type Ca 2+ channels. The antiarrhythmic eects of oestrogens may contribute to the cardioprotective actions of oestrogens.

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