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

biomed - Meyer C , Schueller P , Balzer J , Lauer T , Westenfeld R , Schauerte P , Hennersdorf M , Steiner S , Kelm M , Rassaf , Rassaf T

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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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Chronic kidney disease

Nervous system

Sympathetic

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Publié par	biomed
Publié le	01 janvier 2009
Nombre de lectures	8
Langue	English

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The study was approved by a local Ethics Committee. In a randomized, double-masked, placebo controlled crossover design we studied the impact ofchemosen-sory deactivation on heart rate, blood pressure, and oxygen saturation by 5-min inhalation of100% oxy-gen in 10 ESRD patients and 10 age and gender matched controls. We assessed whether the resting sympathetic tone, as measured by baseline plasma cat-echolamine levels and time-domain heart rate variabili-ty (HRV) parameters, contributes to chemosensory ac-tivation in ESRD resulting in an impaired hyperoxic CHRS. Placebo consisted ofbreathing room air.

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SYMPATHETICHYPERACTIVITYINFLUENCESCHEMOSENSORFUNCTION IN PATIENTS WITHEND-STAGERENALDISEASE

1 11 11 23 C. Meyer , P. Schueller , J. Balzer , T. Lauer , R. Westenfeld , P. Schauerte , M. Hennersdorf, 1 11 S. Steiner , M. Kelm , T. Rassaf

Eur J Med Res (2009) 14(Suppl. IV): 151-155

EUROPEAN JOURNAL OF MEDICAL RESEARCH

Key words:chemoreflexes, end-stage renal disease, nervous system, sympathetic

Abstract Backgr ound:Autonomic neuropathy is common in pa-tients suffering from end-stage renal disease (ESRD). This may in part explain the high cardiovascular mor-tality in these patients. Chemosensory function is in-volved in autonomic cardiovascular control and is mechanistically linked to the sympathetic tone. Objective:The aim ofthe present study was to assess whether sympathetic hyperactivity contributes to an al-tered chemosensory function in ESRD. Material and methods:In a randomized, double-masked, placebo controlled crossover design we stud-ied the impact ofchemosensory deactivation on heart rate, blood pressure and oxygen saturation in 10 ESRD patients and 10 age and gender matched con-trols. The difference in the R-R intervals divided by the difference in the oxygen pressures before and af-ter deactivation ofthe chemoreceptors by 5-min in-halation of7 L oxygen was calculated as the hyperox-ic chemoreflex sensitivity (CHRS). Placebo consisted of breathingroom air. Baseline sympathetic activity was characterized by plasma catecholamine levels and 24-h time-domain heart rate variability (HRV) param-eters. Results:Plasma norepinephrine levels were increased (1.6 ± 0.4 vs. 5.8 ± 0.6; P<0.05) while the SDNN (standard deviation ofall normal R-R intervals: 126.4 ± 19 vs. 100.2 ± 12 ms), the RMSSD (square root of the mean ofthe 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 com-pared to controls. CHRS was impaired in ESRD pa-tients (2.9 ± 0.9 ms/mmHg, P<0.05) as compared to controls (7.9 ± 1.4 ms/mmHg). On multiple regres-sion analysis 24 h-Triangular index, RMSSD, and plas-ma norepinephrine levels were independent predictors of animpaired hyperoxic CHRS. Conclusion:Sympathetic hyperactivity influences che-mosensory function in ESRD resulting in an impaired hyperoxic CHRS.

1 Division ofCardiology, Pulmonology and Angiology, University ofDuesseldorf, 2 Division ofCardiology and Pulmonology, RWTH Aachen University, 3 Medical Clinic I, SLK-Kliniken Heilbronn, Germany

INTRODUCTION Autonomic neuropathy is common in patients with end-stage renal disease (ESRD). This may in part ex-plain the high cardiovascular mortality in these pa-tients [1-4]. The underlying mechanisms ofa sympa-thetic-parasympathetic imbalance in ESRD are still not fully understood. Previous reports demonstrated that sympathetic activation in ESRD involves firing of afferent renal nerve fibres, activation ofthe renin-an-giotensin system, and decreased nitric oxide bioavail-ability [5]. A causal link between tonic chemoreflex ac-tivation and an increased efferent sympathetic activity to muscle circulation has recently been reported [6]. Deactivation ofperipheral chemosensors by inhala-tion ofpure oxygen, leads to sympathetic withdrawal and a subsequent decrease ofheart rate [6, 7]. Impair-ment ofthis desensitization, as a consequence ofton-ic chemoreflex activation, has been demonstrated to be a predictor ofventricular tachyarrhythmias. The hyperoxic cardiac chemoreflex sensitivity (CHRS) re-flects the relative decrease ofR-R intervals during ad-ministration ofconcentrated O2and characterizes the deactivation ofcarotid and/or aortic chemoreceptors. The aim ofthe present study was to assess whether sympathetic hyperactivity influences chemosensory function in ESRD. MATERIAL ANDMETHODS STUDYDESIGN

December 7, 2009

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

Chronic kidney disease

Nervous system

Sympathetic

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