TY - JOUR
T1 - Elevated renal nerve activity after spinal transection
T2 - Effects on renal function
AU - Osborn, J. W.
AU - Livingstone, R. H.
AU - Schramm, L. P.
PY - 1987
Y1 - 1987
N2 - 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.
AB - 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.
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M3 - Article
C2 - 3661757
AN - SCOPUS:0023630634
SN - 0002-9513
VL - 253
SP - 22/4
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 4
ER -