The aim is to study the effect of dimethylsulfoxide-soluble smoking particles (DSP) and nicotine on the contractility of rat mesenteric artery. The superior mesenteric artery segments were cultured with DSP or nicotine for 24 h. The vascular contractibility was recorded with myograph system. DSP 0.4 mL/L and nicotine 0.48 and 0.96 mg/L shifted the concentration-contractile curves induced by sarafotoxin 6c, a selective agonist for $ET_B$ receptor toward the left with increased $E_{max}$. DSP 0.4 mL/L and nicotine 0.96 mg/L shifted $ET_A$ receptor-mediated the concentration-contractile curves toward the left with increased $E_{max}$. However, nicotine 0.06 mg/L which is the equivalent concentration of nicotine in DSP 0.4 mL/L did not affect the curves and the $E_{max}$ mediated with $ET_A$ receptor and $ET_B$ receptor. DSP 0.2 and 0.4 mL/L shifted the concentration-contractile curves induced by noradrenaline toward the right with decreased $E_{max}$. Neither did nicotine 0.06 and 0.96 mg/L. Both DSP and nicotine shifted the concentration-contractile curves induced by 5-hydroxytryptamine (5-HT) toward the right parallely. DSP changed the phenotypes towards an increased efficacy of $ET_A$ receptor and $ET_B$ receptor, and a reduced efficacy of 5-HT receptor and $alpha$-adrenocceptor. The effects of DSP on ETB receptor, ETA receptor and $alpha$-adrenocceptor were independent of nicotine. The effect on 5-HT receptor was responsible to nicotine.