Considering the singular vasomotor behavior of the pulmonary artery, we were interested to test NS-004 (1-(2 -hydroxy-5 -chlorophenyl)-5-trifluoromethyl-2(3H)-benzimidazolone) on pulmonary artery smooth muscle cells. Using the patch clamp technique, we identified a delayed rectifier K + current and a Ca 2 + -activated K + current. With a low free intracellular Ca 2 + concentration ([Ca 2 + ] i ), 10-50 μM NS-004 activated a noisy outward current which was blocked by iberiotoxin. 50 μM NS-004 also inhibited a smooth inactivating outward current. Under these conditions, 10 μM NS-004 induced no change in the resting membrane potential. With a higher free [Ca 2 + ] i , 10 μM NS-004 was 3.5 times more efficacious in increasing the noisy current and it induced a hyperpolarization. We concluded that increasing free [Ca 2 + ] i induced potentiation of the NS-004-induced activation of high conductance Ca 2 + -sensitive K + channels and of the NS-004-induced hyperpolarization of the cell. The delayed rectifier K + channel was inhibited by NS-004 as well as by an increased free [Ca 2 + ] i .