Role of Central Vestibular Pathway on Control of Blood Pressure During Acute Hypotension in Rats

ABSTRACT

BACKGROUND AND OBJECTIVES: Central role of the vestibular system on control of blood pressure and interrelationships between the vestibular nucleus and solitary nucleus during acute hypotension were investigated in bilateral labyrinthectomized (BLX) or sinoaortic denervated (SAD) rats. Changes of electrical activity in the medial vestibular nucleus (MVN), solitary tract nucleus (STN), and rostral ventrolateral medullary nucleus (RVLM) were investigated in rats in while acute hypotension was induced by sodium nitroprusside (SNP). RESULTS: Evoked potential in MVN neuron caused by electrical stimulation of the peripheral vestibular system was composed of 3 waves with latencies of 0.48+/-.10 ms, 1.04+/-.09 ms and 1.98+/-.19 ms. Electrical stimulation to MVN or RVLM increased blood pressure. MVN at the induction of acute hypotension showed excitation in 61% of type I neurons and inhibition in 68% of type II neurons. In STN, acute hypotension produced excitation in 62.1% of neurons recorded in intact labyrinthine animals, inhibition in 72.3% of neurons recorded in BL animals, and excitation in 60% of recorded neurons in SAD animals. In RVLM, acute hypotension produced excitation in 66.7% of neurons recorded in intact labyrinthine animals and inhibition in 64.9% of neurons recorded in BL animals. In spatial distribution of STN neurons responded to acute hypotension, excitatory responses were mainly recorded in rostral and ventral portion, and inhibitory responses were mainly recorded in caudal and lateral portion. In RVLM, excitatory responses were mainly recorded in rostral and dorsomedial portion, and inhibitory responses were mainly recorded in caudal and ventrolateral portion. CONCLUSION: These results suggest that afferent signals from the peripheral vestibular receptors are transmitted to STN through the vestibular nuclei and assist to the baroreceptors for controlling blood pressure following acute hypotension.