Effects of nicorandil on contractile responses to α<sub>1</sub>- and α<sub>2</sub>adrenoceptor agonists were examined in isolated rabbit aorta. Nicorandil (10<sup>–6</sup> or 10<sup>–5</sup> M) inhibited contractile responses to clonidine (CL) and BHT-920 in a concentration-dependent manner, but had no effect on the response to methoxamine (MO). Nifedipine (10<sup>–6</sup> and 10<sup>–5</sup> M) had no significant effect on responses to CL and MO, but it had a noticeable inhibitory effect on the response to BHT-920. In tissues pretreated with phenoxybenzamine, nicorandil (10<sup>–5</sup> M) inhibited the residual response to MO, and nifedipine (10<sup>–5</sup> M) inhibited responses to MO and CL. The relationship between maximum contraction and percent receptor occupancy was found to be nonlinear for MO, but was near linear for CL and BHT-920. The inhibitory effect of prazosin (pA<sub>2</sub> of about 9) on MO and CL was much greater than that of yohimbine (pA<sub>2</sub> of about 6). Nicorandil had no apparent or slight inhibitory effect on responses to potassium and Ca<sup>2+</sup>, and this inhibitory effect was much less than that of nifedipine. These results indicate that the responses induced by MO, CL, and BHT-920 in the rabbit aorta are due to activation of α<sub>1</sub>-adrenoceptors. It is also suggested that nicorandil minimally affects voltage-dependent Ca<sup>2+</sup> influx and that differential effects of nicorandil on the responses to α<sub>1</sub> and α<sub>2</sub> agonists may be the result of differeneces in the amount of receptor reserve that exist for MO, CL, and BHT-920 in this blood vessel.