Inhibition of renal nerve sympathetic activity by spinal stimulation in rat

Abstract

We determined the physiological and anatomical properties of systems mediating renal nerve inhibition elicited by electrical and chemical stimulation of the cervical dorsolateral funiculus of the anesthetized spinally transected rat. Stimulus-response characteristics suggested that this system was well suited for a role in tonic inhibition of sympathetic activity. Inhibition was elicited from a region of the cervical spinal cord extending from a lateral position near the accessory nerve to the dorsal columns. Inhibition could not be elicited by spinal stimulation before lesions had been placed rostral to stimulation sites in the lateral funiculi. Inhibition was blocked by similarly placed lesions caudal to stimulation sites. Therefore, this system may course in the lateral funiculus, and it may be tonically active in intact rats. Renal sympathetic activity could be inhibited by electrical stimulation caudal to large, chronic, spinal lesions. Therefore, some component of the inhibitory system was either antidromically activated or propriospinal. Glutamate applied to the dorsolateral surface of the cervical spinal cord elicited inhibition indistinguishable from that elicited by electrical stimulation, which suggested that neurons with somas located superficially at cervical levels may be responsible for some component of the spinally elicited inhibition.

A Novel Pressor Area at the Medullo-Cervical Junction That Is Not Dependent on the RVLM: Efferent Pathways and Chemical Mediators

“…The rostrocaudal extent of these cell groups beyond 1.2 mm caudal to the caudal pole of the inferior olive groups remains to be determined. It is noteworthy in respect of functional heterogeneity that excitation of the dorsolateral surface of the cervical spinal cord in spinally transected or RVLM-inhibited rats evoked inhibition of the renal nerve, whereas in the intact preparation, sympathoexcitation was evoked (Schramm and Livingstone, 1987;Poree and Schramm, 1992). In this respect, effects of MCPA excitation on sympathetic outflows, other than the cervical sympathetic and splanchnic tested here, will be of interest.…”

Sympathoinhibitory effects of rilmenidine may be mediated by sites located below the brainstem

“…These experiments were designed to confirm the increase in SNS activity previously hypothesized (Sannajust et al, 1992) on of indirect evidence great hypotensive effect of the ganglionic blocker, trimethaphan and to demonstrate whether the ability of rilmenidine to lower BP could be related to the degree of central sympathetic drive. It is generally accepted (Zimpfer et al, 1982;Murthy et al, 1982;Matsukawa & Ninomiya, 1989) Schramm & Livingstone (1987) and Taylor & Schramm (1987), the spinal cord transection profoundly and irreversibly decreased SBP and DBP but less markedly reduced HR. Interestingly, the spinal cord transection did not completely abolish the RSNA which returned to the level observed in conscious SHRs, demonstrating that pentobarbitone-anaesthesia enhances the peripheral SNS tone by a central effect.…”

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

“…SPNs are innervated by direct inputs from supraspinal regions, including the A5 region of the pons, raphe nuclei, paraventricular nucleus, lateral hypothalamus, and rostral ventrolateral medulla (RVLM) (Strack et al, 1989) and also via inputs from propriospinal pathways, which originate in the cervical spinal cord (Schramm and Livingstone, 1987). All these regions may give rise to A2 A R-positive terminals in the IML; however, the RVLM is a particularly likely candidate.…”