Changes In Renal Sympathetic Activity Research Articles

Lateralized changes in renal sympathetic activity evoked by unilateral stimulation of lateral/dorsolateral periaqueductal gray

Periaqueductal gray (PAG) is considered an important synaptic relay for behavioral, thermal and cardiovascular responses to stress. Stimulation of lateral/dorsolateral PAG (l/dl PAG) causes fight/flight reaction and sympathetically mediated cardiovascular changes. In adult male anesthetized rats (n=5), we compared changes in heart rate (HR), mean arterial pressure (MAP) and renal sympathetic activity (RSNA) produced by chemical activation (NMDA 100pmol/100nl) of right (R) and left (L) sides of l/dl PAG. RSNA was recorded only on the L side. We observed greater increases in left RSNA following ipsilateral l/dl PAG stimulation (Δ: L 92±14 vs. R 17±4%; P=0.0012). These responses were accompanied by increases in MAP and HR (average Δ: 17mmHg and 35bpm, respectively), but no differences in the magnitude of these responses were found between left or right l/dl PAG stimulation. Maximal changes in MAP and RSNA occurred at the same time, about 30s after l/dl PAG stimulation. Intriguingly, however, the maximal response for HR was delayed (≈90s), following a different time course. We conclude that the functional descending pathways from l/dl PAG to renal sympathetic nerves are prominently lateralized. The mechanisms involved in the differential time course responses between MAP/RSNA and HR require further investigation. Support: FAPEMIG‐PPM and CNPq.

The renal sympathetic and renin-angiotensin response to lower body negative pressure in well-compensated cirrhosis

Background & Aims: Certain antinatriuretic hormonal systems may be involved in the subclinical sodium handling abnormality in preascitic cirrhosis. The aims of this study were to determine the following in preascitic cirrhosis: (1) basal activity of the renal sympathetic and renin-angiotensin systems and (2) the relationship between the response of these systems to lower body negative pressure and sodium excretion. Methods: Seven preascitic cirrhotic patients and 9 age- and sex-matched controls were studied on a 150 mmol sodium per day diet. Systemic and renal hemodynamics, renal neurohormonal secretion rates, and sodium excretion were assessed before, during increasing levels of, and after lower body negative pressure, each for 30 minutes. Results: Both groups responded with a significant decrease in central venous pressure ( P < 0.01) that remained higher in the cirrhotics than in the controls throughout the study. Cirrhotics showed significant increases compared with controls in renal renin and angiotensin II secretion rates at −20 mm Hg of lower body negative pressure, which was associated with significant renal sodium retention (96 ± 17 μmol/min vs. 218 ± 21 μmol/min at baseline, P < 0.05), but there was no change in renal sympathetic activity. Conclusions: In preascitic cirrhosis, sodium retention occurs in response to lower body negative pressure, which was associated with increased renal renin-angiotensin activity. Stimulation of the intrarenal renin-angiotensin system may be the initial renal pathophysiological change causing sodium retention in cirrhosis. GASTROENTEROLOGY 1998;115:397-405

Changes of Renal Sympathetic Activity in Acute and Chronic Conscious Sinoaortic Denervated Rats

The arterial pressure level attained in sinoaortic denervated rats depends on the net effect of eliminating excitatory and inhibitory influences (chemoreceptor and baroreceptor elimination, respectively). After sinoaortic denervation is completed, the hypertension usually observed within the first few days is followed by normotension at the chronic stages. In this work renal sympathetic nerve activity was measured in conscious, unrestrained rats 6 hours (acute) and 20 days (chronic) after sinoaortic denervation. Increased arterial pressure (154 +/- 10 versus 114 +/- 3 mm Hg in controls) and renal sympathetic nerve activity (32 +/- 5 versus 13 +/- 2 bars per cycle in controls) with no changes in heart rate (404 +/- 17 vs 380 +/- 26 beats per minute) were observed in rats with acute sinoaortic denervation. In rats with chronic sinoaortic denervation, arterial pressure (119 +/- 8 mm Hg) and renal sympathetic nerve activity (13 +/- 6 bars per cycle) returned to control levels. Bradycardiac and tachycardiac responses to changes in blood pressure were reduced to 88% and 89%, respectively, in rats with acute sinoaortic denervation and 76% and 74%, respectively, in rats with chronic sinoaortic denervation. The reflex control of renal sympathetic nerve activity after acute and chronic sinoaortic denervation showed an impairment of sympathoinhibition (0.13 +/- 0.02 and 0.25 +/- 0.1 bars per cycle, respectively, versus 0.9 +/- 0.17 bars per cycle in controls). Sympathoexcitatory responses also were impaired in rats with acute and chronic sinoaortic denervation (0.08 +/- 0.03 and 0.37 +/- 0.1 bars per cycle, respectively, compared with 0.98 +/- 0.2 bars per cycle in controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction between medullary and cervical regulation of renal sympathetic activity

We have reported that electrical or glutamate stimulation of the dorsolateral surface of the cervical spinal cord elicits a 40–60% decrease in renal sympathetic activity (RSA) in anesthetized rats. Because evoked sympatho-inhibition was observed, however, only after transection of the cervical spinal cord at C1, we suggested that unidentified supraspinal neurons affect the regulation of RSA by cervical neurones. In the present experiments, we tested the hypothesis that the modulatory supraspinal neurons are located in the ventrolateral medulla by observing the effects of rostroventral, lateral, medullary (RVLM) injections of the GABAergic agonist, muscimol, on baseline RSA and on our ability to inhibit that activity by cervical stimulation. GABAergic inhibition in the RVLM of chlorolose anesthetized rats elicited changes in RSA that were similar to those observed after transection of the spinal cord, including a 41% decrease in mean arterial pressure and a 44% increase in RSA. Moreover, after muscimol inhibition of RVLM neurons, electrical or glutamate stimulation of the dorsolateral cervical spinal cord elicited a decrease in RSA in otherwise intact rats. These results suggest that neurons in the RVLM interact with neurons in the cervical spinal cord in the regulation of RSA.

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.

Reduction of renal nerve activity by volume expansion in conscious cats.

In conscious cats with intact or denervated baroreceptors volume expansion of 5-15% of blood volume was performed with dextran and isotonic sodium chloride. Renal sympathetic activity (RSA), electroencephalogram (EEG) blood pressure (BP) and heart rate (HR) were recorded. RSA was reduced by 25-85% in 10 experiments out of 11 by volume expansion both with dextran and isotonic sodium chloride. Reduction of RSA could not be related to different states of wakefulness as indicated by the EEG, so could only be caused by volume expansion, although no quantitative correlation could be detected. No differences were observed between animals with intact and denervated baroreceptor. In most experiments BP and HR decreased during volume expansion up to -25 mmHg and up to -23 beats/min, respectively. The degree of BP and HR reduction could not be related to the degree of RSA reduction. The results suggest that changes in RSA might be involved in the renal response to volume expansion.