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.
Material 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.