The loss of labyrinthine inputs in patients or animal models has been demonstrated to affect autonomic regulation. Considerable evidence suggests that vestibular-autonomic responses serve to adjust blood pressure and respiratory activity during movement and postural alterations. However, following peripheral vestibular lesions, compensation rapidly occurs, such that autonomic disturbances are not readily evident in patients with chronic labyrinthine dysfunction. This manuscript summarizes the evidence suggesting that vestibular inputs influence autonomic regulation, but that cardiovascular and respiratory responses linked to movement recover quickly subsequent to the loss of labyrinthine signals. In addition, the clinical implications of dysfunction of vestibulo-autonomic reflexes are described. Furthermore, the mechanisms potentially responsible for the return of the ability to produce posturally-related adjustments in blood pressure and respiration following vestibular lesions are discussed. In particular, evidence that somatosensory signals can replace labyrinthine inputs to vestibular nucleus neurons that participate in autonomic regulation is provided.