Accumulating evidence suggests that steady-state K(+) currents modulate excitability and action potential duration, particularly in cardiac cell types with relatively abbreviated action potential plateau phases. Despite representing potential drug targets, at present these currents and their modulation are comparatively poorly characterized. Therefore, we investigated the effects of phenylephrine [PE; an alpha(1)-adrenoceptor (alpha(1)-AR) agonist] on a sustained outward K(+) current in rat ventricular myocytes. Under K(+) current-selective conditions at 35 degrees C and whole-cell patch clamp, membrane depolarization elicited transient (I(t)) and steady-state (I(ss)) outward current components. PE (10 microM) significantly decreased I(ss) amplitude, without significant effect on I(t). Preferential modulation of I(ss) by PE was confirmed by intracellular application of the voltage-gated K(+) channel blocker tetraethylammonium, which largely inhibited I(t) without affecting the PE-sensitive current (I(ss,PE)). I(ss,PE) had the properties of an outwardly rectifying steady-state K(+)-selective conductance. Acidification of the external solution or externally applied BaCl(2) or quinidine strongly inhibited I(ss,PE). However, I(ss,PE) was not abolished by anandamide, ruthenium red, or zinc, inhibitors of TASK acid-sensitive background K(+) channels. Furthermore, the PE-sensitive current was partially inhibited by external administration of high concentrations of tetraethylammonium and 4-aminopyridine, which are voltage-gated K(+) channel-blockers. Power spectrum analysis of I(ss,PE) yielded a large unitary conductance of 78 pS. I(ss,PE) resulted from PE activation of the alpha(1A)-AR subtype, involved a pertussis toxin-insensitive G-protein, and was independent of cytosolic Ca(2+). These results collectively demonstrate that alpha(1A)-AR activation results in the inhibition of an outwardly rectifying steady-state K(+) current with properties distinct from previously characterized cardiac K(+) channels.