This study investigated the influence of the chronic cerebral dopamine deficiency after 6-hydroxydopamine lesions of dopaminergic mesostriatal system and NO pathways on the length-tension relation in vascular smooth muscles to their distension. Experiments were performed on isolated strips of rat portal vein. The results indicate that the attenuated contraction responses and the increased stiffness of vascular smooth muscles to the distension in a chronic mesostriatal dopamine deficiency. It was found that these responses may be, in part, normalized after a long-term L-arginine administration. The same changes were marked in the responses of intact vascular strips after the inhibition of NО-synthase activity and L-arginine perfusion. It has been suggested that, in a chronic mesostriatal dopamine deficiency, the reduced vascular reactivity was due to the decreasing of NO synthesis by endothelium and L-arginine could be used in the treatment of these vascular disorders.