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The present study has been conducted to evaluate the chronic effects (7 months) of Moxonidine (M) and Amlodipine (A) on lipid profile and urinary sodium excretion in patients with Metabolic Syndrome. Twenty seven obese hipertensive subjects (BMI = 33 ± 1.0, MBP = 124.6 ± 1.6 mmHg, 4 males, 23 females, age 49.3 ± 1.5 yrs) were randomly assigned to receive M [(n = 17), 49.3 ± 1.9 yrs] or A [(n = 10), 48.3 ± 2.4 yrs]. Both A and M caused significant reduction in systolic, diastolic and mean blood pressure (MBP), although no significant difference was observed between the two groups [MBP: M-122.8 ± 1.5 vs 111.2 ± 3.6 mmHg (p = 0.003), A-127.1 ± 2.6 vs 106.0 ± 2.4 (p = 0.0001)]. In conditions of adequate control of sodium and calories intake, the urinary excretion of sodium/creatinine in 12h (NaU) decreased in both groups during blood pressure reduction, but significantly less (p = 0.03) in the M group (21.65 ± 3.992 vs 19.22 ± 2.26 mmol/mmol) when compared to the A group (16.95 ± 2.77 vs 10.92 ± 2.77 mmol/mmol). We observed a significant diminution of energy intake (1987 ± 60, vs 1784 ± 119 calories, p < 0.05), as well as on the waist circumference in the M group (104.4 cm vs 103 cm, p < 0.04), but not in the A group (2229 ± 244 vs 1923 ± 298 calories, p = 0.19 and 100.4 vs 101 cm, p = 0.78). There was a 12% reduction of serum triglycerides concentration with M. Both drugs showed no significant effects on plasma glucose, HDL-C and LDL-C. The administration of M, when compared to A, to obese hypertensive patients reduced the intake of calories, waist circumference and serum triglycerides. Besides having the same antihypertensive efficacy, Moxonidine retained less sodium than Amlodipine.

Normal pregnancy is associated to increased levels of leptin which appears to be exacerbated in preeclampsia. We conducted this study to verify the profile of leptin in adolescents during normal gestation (NG) and pre-eclampsia (PE). We studied 19 adolescents (12–18 yrs of age), 5 who developed PE, and 15 with NG, during the hole gestation. Serum leptin levels were evaluated by radioimmunoassay, and blood pressure (BP) using DINAMAP 1846. Patients who presented BP >140 /90 mmHg and proteinuria >300 mg/24 h, without previous hypertension were considered with PE. To adjust for Body Mass Index (BMI), we used the ratio of leptin to BMI, to compare the evolution in both groups, Leptin levels and BMI increased during NG and PE reaching the highest values after 30 weeks of gestation. During NG, leptin correlated significantly with BMI at 21–30 weeks (r=0.71; p<0.0004) and after 30 weeks of gestation (r=0.94; p<0.0001). These correlations were lost both at 20–30 weeks (r=0.8; p=0.1) and >30 weeks of gestation (r=0.7, p=0.2) in PE. Although leptin levels were not different between groups, the leptin to BMI ratio was significantly lower in NG when compared to PE: 21–30 weeks: 0.44±0.02 and 0.56±0.06 ng/dl (p=0.04), respectively; after 30 weeks: 0.41±0.04 and 0.70±0.15 (p=0.03), respectively. In adolescents, leptin to BMI ratio appears to indicate a higher risk of PE.