Vibration stress and the cellular mechanisms in the autonomic nervous system

The characteristic symptoms of vibration disease, such as Raynaud's phenomenon and palmar superhydrosis, are associated with a sympathetic hyperactivity. This paper discusses the possible sites and mechanisms of the vibration stress-induced facilitation and disinhibition in the sympathetic nervous system, particularly at the levels of the spinal cord and sympathetic ganglion. At the level of the preganglionic neurons, vibration stress may facilitate the activity of the alpha-1 adrenoceptors that mediate the slow excitatory postsynaptic potential and the spike-after depolarization. If the sympathetic hyperactivity is in part due to disinhibition, it could be produced by inhibition of the activity of the alpha-2 adrenoceptors that mediate the slow inhibitory postsynaptic potential in preganglionic neurons. At the level of the ganglion, muscarinic and peptidergic transmission may be facilitated in vibration disease.