“…sites as well as the arterial pressor and depressor responses and that the ICP responses cannot be explained merely by the secondary, transmural action of the BP change evoked by the activation of brainstem sites. Though the net volume changes in any of the intracranial contents within the rigid skull, which are induced by vascular autoregulation of cerebral blood vessels due to metabolic changes (LANGFITT et al, 1965), chemical substances like angiotensin (BARBELLA et al, 1983), and any other causes (LUNDGERG et al, 1968), produce a change in ICP, the rapid changes and reversibility of ICP and the enhancement of the stimulus-induced increase in ICP at the lowered BP level indicate that the ICP responses are primarily caused by alteration in blood volume due to neurogenic dilation and constriction of intracranial vessels, thereby permitting some of the systemic blood pressure to affect the geometry of the vascular bed, as is the case with a possible origin of the plateau waves of ICP (LUNDBERG et al, 1968). The primary neurogenic response of intracranial blood vessels was also proposed in case of electrical stimulation of fastigial nucleus (NAKAI et al, 1983) parasympathetic nerve stimulation (D'ALECY and ROSE, 1977) and sympathetic nerve stimulation (WEI et al, 1975;AUER et al, 1983;BAUMBACH and HEISTAD, 1983).…”