The basic mechanism for the excitation of the peripheral vestibular receptors following acute hypotension induced by sodium nitroprusside (SNP) or hemorrhage was investigated in anesthetized rats. Electrical activity of the afferent vestibular nerve was measured after pretreatment with kynurenic acid, an NMDA receptor antagonist. The activity of the vestibular nerve at rest following acute hypotension induced by SNP or simulating hemorrhage was a greater increase than in control animals. The gain of the vestibular nerve with sinusoidal rotation following acute hypotension increased significantly compared to control animals. The acute hypotension induced by SNP or hemorrhage did not change the activity of the afferent vestibular nerve after kynurenic acid injection. These results suggest that acute hypotension produced excitation of the vestibular hair cells via glutamate excitotoxicity in response to ischemia.