Augmentation of the delayed rectifier potassium current by ET A endothelin receptor in guinea pig atrial myocytes

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.