Vascular tone is mainly regulated by the activities of voltage-dependent Ca²⁺ channels (VDCCs) and large-conductance Ca²⁺-activated K⁺ (BK_Ca) channels in smooth muscles. We previous reported that pimaric acid and 12,14-dichlorodehydroabietic acid (DiCl-DHAA) activated BK_Ca channels and blocked VDCCs. However, the effects of these compounds on contractile response of vascular smooth muscles are undetermined. In the present study, we examined the effects of pimaric acid, DiCl-DHAA, and abietic acid on contraction of rat pulmonary artery. High K⁺ (40 mM)-induced vasocontraction was reduced by pimaric acid or DiCl-DHAA in a concentration-dependent manner (3-30 mM). Endothelin 1 (10 nM)-induced vasocontraction was also attenuated by pimaric acid or DiCl-DHAA (30 mM). Unexpectedly, their relaxation effects were not blocked by the pretreatment with a BK_Ca channel blocker, paxilline (1 mM). Quantitative real-time PCR data revealed that the α/β1 subunits of BK_Ca channel and Cav1.2/β2/β3 subunits of VDCC were abundantly expressed in rat pulmonary arterial smooth muscles. These results indicate that relaxing action by pimaric acid and DiCl-DHAA is mediated by VDCC inhibition rather than BK_Ca channel activation in rat pulmonary arterial smooth muscles.