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      Sympathetic hyperactivity influences chemosensor function in patients with end-stage renal disease

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      Author(s): 1 , , 1 , 1 , 1 , 1 , 2 , 3 , 1 , 1 , 1
      Publication date (Electronic):
      Journal: European Journal of Medical Research
      Publisher: BioMed Central
      Conference name: International Conference 'Advances in Pneumology’
      Conference date: 12-14 June 2009
      Keywords: chemoreflexes, end-stage renal disease, nervous system, sympathetic

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          Abstract

          Background

          Autonomic neuropathy is common in patients suffering from end-stage renal disease (ESRD). This may in part explain the high cardiovascular mortality in these patients. Chemosensory function is involved in autonomic cardiovascular control and is mechanistically linked to the sympathetic tone.

          Objective

          The aim of the present study was to assess whether sympathetic hyperactivity contributes to an altered chemosensory function in ESRD.

          Materials and methods

          In a randomized, double-masked, placebo controlled crossover design we studied the impact of chemosensory deactivation on heart rate, blood pressure and oxygen saturation in 10 ESRD patients and 10 age and gender matched controls. The difference in the R-R intervals divided by the difference in the oxygen pressures before and after deactivation of the chemoreceptors by 5-min inhalation of 7 L oxygen was calculated as the hyperoxic chemoreflex sensitivity (CHRS). Placebo consisted of breathing room air. Baseline sympathetic activity was characterized by plasma catecholamine levels and 24-h time-domain heart rate variability (HRV) parameters.

          Results

          Plasma norepinephrine levels were increased (1.6 ± 0.4 vs. 5.8 ± 0.6; P < 0.05) while the SDNN (standard deviation of all normal R-R intervals: 126.4 ± 19 vs. 100.2 ± 12 ms), the RMSSD (square root of the mean of the squared differences between adjacent normal R-R intervals: 27.1 ± 8 vs. 15.7 ± 2 ms), and the 24-h triangular index (33.6 ± 4 vs. 25.7 ± 3; each P < 0.05) were decreased in ESRD patients as compared to controls. CHRS was impaired in ESRD patients (2.9 ± 0.9 ms/mmHg, P < 0.05) as compared to controls (7.9 ± 1.4 ms/mmHg). On multiple regression analysis 24 h-Triangular index, RMSSD, and plasma norepinephrine levels were independent predictors of an impaired hyperoxic CHRS.

          Conclusion

          Sympathetic hyperactivity influences chemosensory function in ESRD resulting in an impaired hyperoxic CHRS.

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          Sympathetic overactivity in patients with chronic renal failure.

          R Converse, T Jacobsen, R Toto … (1992)
          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. 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 sympathetic-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 +/- 14 mm Hg, P < 0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. 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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            Sympathetic hyperactivity in chronic kidney disease: pathogenesis, clinical relevance, and treatment.

            Gerry Ligtenberg, Marlise Klein, Peter J. Blankestijn … (2004)
            Cardiovascular morbidity and mortality importantly influence live expectancy of patients with chronic renal disease (CKD). Traditional risk factors are usually present, but several other factors have recently been identified. There is now evidence that CKD is often characterized by an activated sympathetic nervous system. This may contribute to the pathogenesis of renal hypertension, but it may also adversely affect prognosis independently of its effect on blood pressure. The purpose of this review is to summarize available knowledge on the role of the sympathetic nervous system in the pathogenesis of renal hypertension, its clinical relevance, and the consequences of this knowledge for the choice of treatment.
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              Reduction of sympathetic hyperactivity by enalapril in patients with chronic renal failure.

              P. Oey, Gezina Oei, F. Boomsma … (1999)
              Inhibition of angiotensin-converting enzyme (ACE) reduces the risk of cardiovascular problems in patients with chronic renal failure. This effect may be due in part to a decrease in sympathetic nervous activity, but no direct evidence of such an action is available. We studied muscle sympathetic-nerve activity in 14 patients with hypertension, chronic renal failure, and increased plasma renin activity before, during, and after administration of the ACE inhibitor enalapril. Ten other patients with similar clinical characteristics were studied before and during treatment with the calcium-channel blocker amlodipine. Normal subjects matched for age and weight were included in both studies. At base line, mean (+/-SD) muscle sympathetic-nerve activity was higher in the group of patients who received enalapril than in the control subjects (35+/-17 vs. 19+/-9 bursts per minute, P=0.004). The baroreflex curve, which reflects changes in muscle sympathetic-nerve activity caused by manipulations of blood pressure with sodium nitroprusside and phenylephrine, was shifted to the right in the patients, but baroreflex sensitivity was similar to that in the control subjects (-2.1+/-1.9 and -2.7+/-1.3 bursts per minute per mm Hg, respectively; P=0.36). A single dose of the sympatholytic drug clonidine caused a greater fall in blood pressure in the patients than in the control subjects. Treatment with enalapril normalized blood pressure and muscle sympathetic-nerve activity (at 23+/-10 bursts per minute) in the patients and shifted the baroreflex curve to the left, reflecting normal blood-pressure levels, without significantly changing sensitivity (-2.3+/-1.8 bursts per minute per mm Hg, P=0.96). In the patients who received amlodipine, treatment also lowered blood pressure but increased muscle sympathetic-nerve activity, from 41+/-19 to 56+/-14 bursts per minute (P=0.02). Increased sympathetic activity contributes to hypertension in patients with chronic renal disease. ACE inhibition controls hypertension and decreases sympathetic hyperactivity.
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                Author and article information

                Conference
                Journal ID (nlm-ta): Eur J Med Res
                Journal ID (iso-abbrev): Eur. J. Med. Res
                Title: European Journal of Medical Research
                Publisher: BioMed Central
                ISSN (Print): 0949-2321
                ISSN (Electronic): 2047-783X
                Publication date Collection: 2009
                Publication date (Electronic): 7 December 2009
                Volume: 14
                Issue: Suppl 4
                Pages: 151-155
                Affiliations
                [1 ]Division of Cardiology, Pulmonology and Angiology, University of Duesseldorf
                [2 ]Division of Cardiology and Pulmonology, RWTH Aachen University
                [3 ]Medical Clinic I, SLK-Kliniken Heilbronn, Germany
                Article
                Publisher ID: 2047-783X-14-S4-151
                DOI: 10.1186/2047-783X-14-S4-151
                PMC ID: 3521372
                PubMed ID: 20156747
                SO-VID: 48972861-5b9a-4ba8-8401-94199c2c2e5e
                Copyright © Copyright ©2009 I. Holzapfel Publishers
                Conference name: International Conference 'Advances in Pneumology’
                Conference location: Leipzig, Germany
                Conference date: 12-14 June 2009
                History
                Categories
                Subject: Research

                ScienceOpen disciplines: Medicine
                Keywords: sympathetic,chemoreflexes,nervous system,end-stage renal disease
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: sympathetic, chemoreflexes, nervous system, end-stage renal disease

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