Effects of moxonidine on sympathetic nerve activity in patients with end-stage renal disease

Journal of Hypertension
Martin HausbergLars Christian Rump

Abstract

End-stage renal disease (ESRD) is characterized by markedly increased sympathetic outflow that contributes to increased cardiovascular mortality in these patients. The central sympatholytic drug moxonidine (MOX) has been shown to reduce muscle sympathetic nerve activity (MSNA) in initial stages of chronic kidney disease; however, the effects in ESRD are not known. The aim of this study was to test the hypothesis that low-dose MOX causes sustained decreases in sympathetic outflow in ESRD patients. Twenty-three ESRD patients (mean age 46.4 +/- 16 years, 14 men, seven women, no diabetic patients) were randomized to a daily treatment of 0.3 mg MOX or placebo (PLA) in addition to pre-existing antihypertensive therapy. At baseline and after 1 and 6 months of treatment, heart rate (HR, ECG), blood pressure (mean arterial pressure, automatic sphygmanometer), calf blood flow (CBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA) (microneurography at the peroneal nerve) were measured. Data are mean +/- SEM. MOX acutely decreased MSNA within 2 h after oral intake (from 45 +/- 3.7 to 35 +/- 3.9 bursts/min, P < 0.05). This decrease was sustained over 6 months (MSNA 45 +/- 3.7, 35 +/- 4.6, 33 +/- 4.5 bursts/min at ...Continue Reading

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