Key result
12-week open-label sibutramine decreased body weight by 4.1 kg and MSNA by 17 bursts/min, and the change in blood pressure inversely correlated with initial MSNA (r2=0.34; P<0.01).
Why the study?
Does baseline sympathetic vasomotor tone determine the blood pressure response to long-term sibutramine treatment in obese subjects?
Does baseline sympathetic vasomotor tone determine the blood pressure response to long-term sibutramine treatment in obese subjects?
In obese subjects, the blood pressure response to sibutramine is inversely related to baseline sympathetic nerve activity, suggesting a central sympatholytic effect.
May identify obese patients likely to lower BP with sibutramine via baseline MSNA; leaves open confirmation in randomized trials.
CONTEXT: The serotonin and norepinephrine transporter inhibitor sibutramine is a widely used antiobesity drug. In acute studies, the peripheral sympathomimetic effect of sibutramine was counteracted by a central sympatholytic action. OBJECTIVE: The objective was to test the hypothesis that blood pressure responses to long-term sibutramine therapy may be related to sympathetic nerve traffic before treatment in a prospective open-label study in an academic clinical research center. PATIENTS: This study comprised 20 obese subjects (body mass index, 30-40 kg/m2; age, 30-57 yr) receiving 5 d of placebo treatment followed by open-label 15 mg/d sibutramine and hypocaloric diet over 12 wk. MAIN OUTCOME MEASURES: Body weight, blood pressure, heart rate, muscle sympathetic nerve activity (MSNA) (microneurography), plasma catecholamines, and adipose tissue gene expression were measured. RESULTS: Open-label sibutramine treatment decreased body weight 4.1 kg (P<0.01) and MSNA 17 bursts per minute (P=0.001), and increased diastolic blood pressure 3 mm Hg (P<0.05) and heart rate 8 bpm (P<0.01). The change in blood pressure with sibutramine treatment was inversely correlated with initial MSNA (r2=0.34; P<0.01). Chronic sibutramine treatment increased adrenoreceptor gene expression and plasma catecholamines. CONCLUSIONS: The blood pressure response to sibutramine treatment is related to initial MSNA so that subjects with higher MSNA exhibit a smaller increase or even a decrease in blood pressure. The phenomenon might be explained by a sustained reduction in central sympathetic activity with sibutramine treatment.
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Heusser et al. (2007) studied Obesity (n=20). Sibutramine vs. Baseline / Placebo was evaluated on Body weight, blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), plasma catecholamines, and adipose tissue gene expression. 12-week open-label sibutramine decreased body weight by 4.1 kg and MSNA by 17 bursts/min, and the change in blood pressure inversely correlated with initial MSNA (r2=0.34; P<0.01).
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