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