Attenuation in the vasodilatory effects of a new synthesized opener of ATP-sensitive K' channels on isolated aorta strips of rat has been shown under experimental (streptozocin-induced) diabetes mellitus. The level of that attenuation depended on the nature of initial vasoconstriction. The most pronounced decrease--43.34% as compared to the control responses in healthy rats, we observed after norepinephrine-induced vasoconstriction. Following preliminary angiothensin-induced vasoconstriction and potassium depolarization, attenuation in vasoconstriction was 20.37% and 22.4%, respectively. Norepinephrine inhibited vasodilator effects of phlocalin in the aorta of diabetic rats much more significantly, as compared to those after potassium depolarization. Inhibitory effects of angiothensin II in rats with diabetes mellitus did not differ from those in the control rats. At the same time, constrictory responses to biological active agents were preserved and they did not differ from those in control rats. We suggest that impairment in vascular reactivity under diabetes mellitus, at least in part, depends on the changes in the functioning of ATP-sensitive potassium channels.