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Biomedical subjects

R H Livingstone

Publications and source records attributed to R H Livingstone.

3 recordsLinked to original sources
PubMed1987

Inhibition of renal nerve sympathetic activity by spinal stimulation in rat.

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.

Analysis of Variance↗
PubMed1987

Elevated renal nerve activity after spinal transection: effects on renal function.

Spinal transection approximately doubles renal sympathetic activity (RSA) in rats. These experiments localized spinal pathways inhibiting RSA and determined the effects of transection-elicited renal sympathetic hyperactivity on renal circulation and renal function. Experiments were conducted in chloralose-anesthetized, paralyzed, artificially respired, male Sprague-Dawley rats. RSA was measured from an electrode on the left renal nerve. Renal arterial blood flow (RABF), glomerular filtration rate, urine flow rate, and renal sodium and potassium excretions were also measured. Localized lesions of the cervical spinal cord indicated that spinal generators of RSA were inhibited by pathways descending in the dorsal cervical cord. Autoregulation of RABF prevented transection-elicited increases in RSA from affecting renal vascular resistance. Renal sodium and potassium excretions were dramatically reduced after spinal transection, although these reductions were ameliorated somewhat by fixing posttransection renal arterial pressure at pretransection levels. We conclude that the vascular effects of transection-elicited elevations in RSA are minimized by autoregulation of RABF and that posttransection changes in renal function result from changes in both arterial pressure and RSA.

Animals↗