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

Abstract

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.

Identification of the spinal pathways involved in the recovery of baroreflex control after spinal lesion in the rat using pseudorabies virus

“…In the rat, a complete spinal transection removes only supraspinal regulation of the sympathetic activity. In the spinally intact rat, tonically active sources of descending inhibition suppress spinal sources of activity to thereby suppress the spinally generated sympathetic activity, whereas, in the transected rat, spinal sources of activity are unimpeded (21,26). Thus, even after acute right hemisection in rats with chronic left hemisection, basal sympathetic outflow driven by spinal sources exists.…”

Sympathoexcitation to intravenous interleukin-1β is dependent on forebrain neural circuits

“…First, activity persists in sympathetic nerves after acute cervical spinal transection (20,23,31), demonstrating that spinal neural circuits can generate efferent sympathetic nerve activity. Second, acute heat stress, which provides a potent stimulus to the sympathetic nervous system in animals with an intact neuraxis (17,19,20), produces renal and splenic sympathoexcitation in spinal cord-transected rats (20), demonstrating that spinal neural circuits are respon- sive to specific experimental interventions.…”

“…At least three possibilities can be considered. First, because intrathecal IL-1␤ administration increases spinal cord blood flow (24) and because cultured rat sympathetic neurons express IL-1 receptors (1,11) and activity persists in sympathetic nerves after cervical spinal cord transection (23,31), spinal and/or ganglionic circuits, in the absence of supraspinal neural circuits, may mediate SND responses to intravenous IL-1␤. Second, because the brain stem (area postrema and perivascular cells in the ventrolateral medulla) contains IL-1␤ receptors (9) and is known to play an important role in sympathetic nerve regulation (2,21,27,28), it may be that brain stem and spinal neural circuits, in the absence of forebrain nuclei, are capable of mediating SND responses to intravenous IL-1␤.…”

Spinal regions involved in baroreflex control of renal sympathetic nerve activity in the rat

“…The spinal pathways mediating ongoing sympathetic activity in the rat (15,35,36,38) cat (12,(17)(18)(19), and human (13) have been well described. Although some evidence from postmortem studies in humans indicates that spinal sympathetic pathways are relatively diffuse (34), others have concluded that these pathways are more concentrated in the dorsolateral white matter (13).…”

“…We have previously shown that ongoing RSNA increases after dorsal hemisection in rats (35,37) due to reduced descending inhibition of spinal sympathetic systems. Therefore, we asked whether spinal lesions might degrade baroreceptor efficacy by reducing the ability of a baroreceptor to decrease RSNA at elevated AP.…”