Abstract
The role of ETA endothelin receptor (ETAR) in the regulation of the delayed rectifier potassium current (IK) was examined in guinea pig atrial myocytes. Application of ET-1 (10 nM) together with an ETB-receptor-selective antagonist, BQ-788 (300 nM), significantly increased the voltage-dependent activation of IK without affecting its half-activation voltage or the slope factor, while it suppressed the calcium current (ICaL) and displaced the time-independent background current to the outward direction. The data suggests that the augmentation of IK contributes to the ETA-receptor-mediated shortening of action potential duration, and hence to the negative inotropic response, in atria.
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