The role of peripheral vestibular receptors in acute hypotension was investigated in anesthetized rats. Acute hypotension was induced by either intravenous infusion of sodium nitroprusside (SNP) or by experimental hemorrhage, and electrical activity and expression of cFos-like immunoreactive (cFL) protein were measured in the medial vestibular nuclei (MVN). Blood pressure decreased proportionately to the does of intravenous SNP and to the volume of the hemorrhage. Blood pressure decreased 10, 30, 50% for the 5, 10, 15μg/kg SNP injection, respectively, and also decreased 30 and 50% after 1- and 2-ml blood loss, respectively, due to hemorrhage. In animals with intact labyrinths, acute hypotension induced by either intravenous infusion of SNP or hemorrhage produced different electrical activities with three different patterns in type I and II neurons of MVN. The responses of type I neurons showed excitatory in 2/3 of recorded neurons and inhibitory or no change in 1/3 of neurons, while the responses of type II neurons showed inhibitory in 2/3 of recorded neurons and excitatory or no change in 1/3 of neurons. In unilateral labyrinthectomized animals, 2/3 of type I neurons ipsilateral to the lesion showed an inhibitory response, and 2/3 of contralateral type I neurons showed an excitatory response after the induction of acute hypotension. The response patterns of type II neurons were opposite from those of the type I neurons. After 30% decrease in blood pressure, cFL protein expressed in the bilateral vestibular nuclei of control animals with intact labyrinths. Expression of cFL protein increased significantly proportionately to the reduction of blood pressure. The unilateral labyrinthectomized animals with acute hypotension produced expression of cFL neurons in contralateral vestibular nuclei to the lesion side, but not in ipsilateral vestibular nuclei. However, cFL protein was not expressed in bilateral vestibular nuclei after acute hypotension in bilateral labyrinthectomized animals. These results suggest that the peripheral vestibular receptors might play a significant role in controlling blood pressure following acute hypotension via activation of type I neurons and inhibition of type II neurons in the vestibular nuclei.