In experiments on isolated preparations of segments of the aorta and portal vein, we demonstrated that endothelium-dependent reactions of vascular smooth muscles (SMs) are suppressed in rats subjected to destruction of the nigro-striatal dopaminergic system in the left hemisphere (model of hemiparkinsonims). Under such conditions, the amplitude of relaxation of SMs of the wall of the thoracic aorta upon the action of the endothelium-dependent vasodilator acetylcholine iodide was four times smaller, while the latency demonstrated a 3.5-fold increase, as compared with the control. The amplitude of relaxation of vascular SMs after application of the endothelium-independent vasodilator sodium nitroprusside remained practically unchanged. In addition, preliminary stretching-induced increments of the amplitude of phasic contractions of the portal vein demonstrated a 2.5-fold decrease; this increment reached the maximum at smaller additional loadings, while the rigidity of the vascular wall increased. In animals that obtained a preparation of coenzyme Q10 (10 mg/kg) with food during one month, contractile reactions of vascular SMs partly recovered. The amplitude of endothelium-dependent relaxation of the aorta increased, the latency of this reaction shortened, stretching-induced increments of the amplitude of phasic contractions increased, and the rigidity of the vascular wall dropped. We conclude that the functional state of the endothelium is worsened, and the vascular reactivity is modified under conditions of chronic insufficiency of nigro-striatal dopamine. It seems probable that oxidative stress is one of the main reasons for such changes. Coenzyme Q10 significantly normalized abnormal vascular reactions (perhaps, due, to a considerable extent, to its antioxidant properties).