Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVL

Somatic and visceral inputs to neurons of the rostral ventrolateral medulla

Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play an essential role in the generation of basal sympathetic tone and in the reflex regulation of blood pressure. In this study responses of RVLM "cardiovascular" neurons to somatic and visceral afferent stimulation were investigated. The activity of 34 RVLM neurons was recorded in urethan-anesthetized paralyzed and artificially ventilated rats. These neurons were identified as cardiovascular based on their baroreceptor sensitivity and their pulse-synchronous discharge. Electrical stimulation of the sciatic nerve excited 31 of the 34 RVLM units (91%). Renal nerve stimulation inhibited firing of 14 of 22 RVLM neurons tested (64%), not affecting the remaining 8 units. Stimulation of splenic nerves inhibited the discharge of 7 of 12 RVLM neurons tested (58%), whereas the remaining 5 units were not affected. All RVLM units responsive to visceral afferent stimulation were also responsive to sciatic nerve stimulation. These results indicate that RVLM cardiovascular neurons receive somatic and visceral inputs, suggesting an involvement of these units in the integration of homeostatic responses to changes in the internal and external environmen