Sympathetic overactivity in patients with chronic renal failure

Richard L. Converse, Tage N. Jacobsen, Robert D. Toto, Charles M T Jost, Frank Cosentino, Fetnat Fouad-Tarazi, Ronald G. Victor

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Abstract

Background. Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. Methods. We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. Results. The mean (±SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58±3 vs. 23±3 bursts per minute, P<0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21±6 bursts per minute) and the normal subjects. The rate of sympa thetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P<0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45±4 vs. 22±4 units, P<0.05) and mean arterial pressure (106±4 vs. 76±14mm Hg, P<0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. Conclusions. Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

Original languageEnglish (US)
Pages (from-to)1912-1918
Number of pages7
JournalNew England Journal of Medicine
Volume327
Issue number27
StatePublished - 1992

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Chronic Kidney Failure
Nephrectomy
Renal Dialysis
Hypertension
Kidney
Peroneal Nerve
Patient Discharge
Sympathetic Nervous System
Microelectrodes
Renin
Vascular Resistance
Blood Vessels
Norepinephrine
Arterial Pressure
Skeletal Muscle

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Converse, R. L., Jacobsen, T. N., Toto, R. D., Jost, C. M. T., Cosentino, F., Fouad-Tarazi, F., & Victor, R. G. (1992). Sympathetic overactivity in patients with chronic renal failure. New England Journal of Medicine, 327(27), 1912-1918.

Sympathetic overactivity in patients with chronic renal failure. / Converse, Richard L.; Jacobsen, Tage N.; Toto, Robert D.; Jost, Charles M T; Cosentino, Frank; Fouad-Tarazi, Fetnat; Victor, Ronald G.

In: New England Journal of Medicine, Vol. 327, No. 27, 1992, p. 1912-1918.

Research output: Contribution to journalArticle

Converse, RL, Jacobsen, TN, Toto, RD, Jost, CMT, Cosentino, F, Fouad-Tarazi, F & Victor, RG 1992, 'Sympathetic overactivity in patients with chronic renal failure', New England Journal of Medicine, vol. 327, no. 27, pp. 1912-1918.
Converse RL, Jacobsen TN, Toto RD, Jost CMT, Cosentino F, Fouad-Tarazi F et al. Sympathetic overactivity in patients with chronic renal failure. New England Journal of Medicine. 1992;327(27):1912-1918.
Converse, Richard L. ; Jacobsen, Tage N. ; Toto, Robert D. ; Jost, Charles M T ; Cosentino, Frank ; Fouad-Tarazi, Fetnat ; Victor, Ronald G. / Sympathetic overactivity in patients with chronic renal failure. In: New England Journal of Medicine. 1992 ; Vol. 327, No. 27. pp. 1912-1918.
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abstract = "Background. Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. Methods. We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. Results. The mean (±SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58±3 vs. 23±3 bursts per minute, P<0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21±6 bursts per minute) and the normal subjects. The rate of sympa thetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P<0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45±4 vs. 22±4 units, P<0.05) and mean arterial pressure (106±4 vs. 76±14mm Hg, P<0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. Conclusions. Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.",
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AU - Toto, Robert D.

AU - Jost, Charles M T

AU - Cosentino, Frank

AU - Fouad-Tarazi, Fetnat

AU - Victor, Ronald G.

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N2 - Background. Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. Methods. We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. Results. The mean (±SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58±3 vs. 23±3 bursts per minute, P<0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21±6 bursts per minute) and the normal subjects. The rate of sympa thetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P<0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45±4 vs. 22±4 units, P<0.05) and mean arterial pressure (106±4 vs. 76±14mm Hg, P<0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. Conclusions. Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

AB - Background. Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. Methods. We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. Results. The mean (±SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58±3 vs. 23±3 bursts per minute, P<0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21±6 bursts per minute) and the normal subjects. The rate of sympa thetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P<0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45±4 vs. 22±4 units, P<0.05) and mean arterial pressure (106±4 vs. 76±14mm Hg, P<0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. Conclusions. Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

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