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Sanjuliani AF et al.  
Effects of Moxonidine on the Sympathetic Nervous System, Blood Pressure, Plasma Renin Activity, Plasma Aldosterone, Leptin, and Metabolic Profile in Obese Hypertensive Patients

Journal of Clinical and Basic Cardiology 2004; 7 (1-4): 19-25

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Fig. 1: Moxonidine - Clinical evaluation Fig. 2: Moxonidine - Effect

Keywords: HypertonieKardiologieKatecholamineMoxonidinplasmacardiologyhypertensionplasma catecholamines

Obesity accounts for around 70 % of the patients with primary hypertension. This association accentuates the risk of cardiovascular disease as it is frequently accompanied by the components of the metabolic syndrome. Clinical, epidemiological and experimental studies show an association between obesity-hypertension with insulin resistance and increased sympathetic nervous system activity. We conducted the present study to evaluate in forty obese hypertensives of both genders, aged 27 to 63 years old, the chronic effects of moxonidine a selective imidazoline receptor agonist on blood pressure, plasma catecholamines, leptin, renin-angiotensin aldosterone system and components of the metabolic syndrome. It was a randomized parallel open study, amlodipine was used as the control drug. Our results show that moxonidine and amlodipine significantly reduced blood pressure without affecting heart rate when measured by the oscillometric method and with twenty-four-hour blood pressure monitoring. Moxonidine therapy decreased systolic blood pressure from 160.4 2.4 to 142.1 3.3 mmHg (p < 0.005) and diastolic blood pressure from 102.4 1.3 to 89.7 1.6 mmHg (p < 0.005) after 24 weeks of treatment. Neither moxonidine nor amlodipine affected normal circadian variations on blood pressure. There was a reduction of the supine arterial plasma levels adrenaline from 63.2 6.6 to 49.0 6.7 pg/ml (p < 0.005), supine arterial levels noradrenaline from 187.9 10.7 to 149.7 13.2 pg/ml (p < 0.01) and orthostatic venous levels of noradrenaline from 258.6 25.0 to 190.3 16.4 pg/ml (p = 0.03) after moxonidine. These variables were not changed by amlodipine. Plasma leptin levels and plasma insulin after 120 min glucose load decreased after moxonidine from 27.2 3.5 to 22.6 2.9 pg/ml (p < 0.05) and from 139.7 31.2 to 76.0 15.2 U/ml (p < 0.05), respectively. However, amlodipine did not modify these variables. There were no alterations in plasma renin activity, and plasma aldosterone after moxonidine, although amlodipine significantly increased the plasma renin activity from 31.4 4.6 to 47.7 5.6 ng/ml/h (p = 0.03). Moxonidine and amlodipine had no significant effect on the other variables. This study shows a comparable reduction of blood pressure with both antihypertensive drugs. Moxonidine decreased sympathetic nervous activity, improved insulin resistance and reduced the plasma levels of leptin.
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