The vestibular system participates in cardiovascular regulation during postural changes. In prior studies, transection of the vestibular nerves resulted in instability in blood pressure during nose-up body tilts, particularly when no visual information reflecting body position in space was available. However, recovery of orthostatic tolerance occurred within a week, presumably because the vestibular nuclei integrate a variety of sensory inputs reflecting body location. The present study tested the hypothesis that lesions of the vestibular nuclei result in persistent cardiovascular deficits during orthostatic challenges. Blood pressure and heart rate were monitored in 5 conscious cats during nose-up tilts of varying amplitude both before and following chemical lesions of the vestibular nuclei. Prior to lesions, blood pressure remained relatively stable during tilts. In all animals, the blood pressure responses to nose-up tilts were altered by damage to the medial and inferior vestibular nuclei; these effects were noted both when animals were tested in the presence and absence of visual feedback. In 4 of the 5 animals, the lesions also resulted in augmented heart rate increases from baseline values during 60° nose-up tilts. These effects persisted for longer than a week, but gradually resolved over time except in the animal with the worst deficits. These observations suggest that recovery of compensatory cardiovascular responses following loss of vestibular inputs is accomplished at least in part through plastic changes in the vestibular nuclei and the enhancement of the ability of vestibular nucleus neurons to discriminate body position in space by employing nonlabyrinthine signals.