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Title: [Effects of sex hormones on HERG potassium channels expressed in Xenopus oocytes]. Author: Osypenko VM, Dehtiar VIe, Naĭd'onov VH, Shuba IaM. Journal: Fiziol Zh (1994); 2001; 47(2):24-31. PubMed ID: 11392110. Abstract: The repolarisation phase of cardiac action potential is characterized by sexual dimorphism suggesting the role of sex steroid hormones in the regulation of K+ channels. Here we report on the effects of testosterone and 17 beta-estradiol on HERG-encoded K+ channels, expressed in Xenopus oocytes. At 1M concentration testosterone decreased the amplitude of HERG-directed IKr (rapid component of cardiac delayed rectifier K+ current) by 30% within 30 min of exposure, while 17-estradiol had no effect. Testosterone did not alter the HERG channels kinetics, voltage-dependence, steady-state activation and inactivation properties suggesting that its action most probably involves the decrease of channels open probability and/or the level of their expression. The signaling pathways mediating testosterone-induced down-regulation of HERG channels in Xenopus oocytes remains to be elucidated. The effect of testosterone on HERG channels in Xenopus oocytes is opposite to what one might expect from shorter cardiac action potential duration and electrocardiographic QT-interval in males compared to females.[Abstract] [Full Text] [Related] [New Search]