Effect of a high-calcium energy-reduced diet on abdominal obesity and cardiometabolic risk factors in obese Brazilian subjects.

BACKGROUND: Clinical trials designed to examine the effects of calcium supplementation on abdominal obesity have had ambiguous results. AIMS: This study aimed to evaluate, during energy restriction, the effects of a high-calcium diet (HCD) on measures of abdominal obesity and cardiometabolic risk factors in Brazilian obese subjects of multiethnic origin. METHODS: We conducted a randomised clinical trial. Fifty obese subjects of both sexes, aged 22-55 years, with stable body weight and a low calcium intake were randomised into the following outpatient dietary regimens: (i) a low-calcium diet (LCD; < 500 mg/day) or (ii) a HCD [1200-1300 mg/day, supplemented with non-fat powdered milk (60 g/day)]. Both groups followed an energy-restricted diet (-800 kcal/day) throughout the study (16 weeks). RESULTS: Thirty-nine participants completed the study. After 16 weeks of energy restriction, a significant reduction was observed in all anthropometric parameters, metabolic variables (except for high-density lipoprotein cholesterol) and blood pressure levels in both the groups. Insulin was significantly reduced only in the HCD group. Subjects on the HCD compared with those on the LCD exhibited a greater reduction in waist circumference (p = 0.002), waist-to-hip ratio (p = 0.0001), diastolic blood pressure (p = 0.04) and mean blood pressure (p = 0.03). CONCLUSIONS: Our study suggests that increased calcium intake may enhance the beneficial effects of energy restriction on abdominal obesity and blood pressure.

Selective imidazoline agonist moxonidine in obese hypertensive patients.

Obesity is the major risk factor for the development of hypertension. This association accentuates the risk of cardiovascular disease, as it is frequently accompanied by the components of the metabolic syndrome. This randomised open parallel study evaluated the chronic effects of moxonidine--a selective imidazoline receptor agonist--on blood pressure, plasma catecholamines, leptin, insulin and components of the metabolic syndrome in obese hypertensives. Amlodipine was used as the control drug. Our results showed that moxonidine and amlodipine significantly reduced blood pressure when measured using the oscillometric method and 24-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. Moxonidine administration reduced the supine arterial plasma levels of adrenaline from 63.2 +/- 6.6 to 49.0 +/- 6.7 pg/ml (p < 0.005), the supine arterial plasma levels of noradrenaline from 187.9 +/- 10.7 to 149.7 +/- 13.2 pg/ml (p < 0.01) and the orthostatic venous plasma levels of noradrenaline from 258.6 +/- 25.0 to 190.3 +/- 16.4 pg/ml (p = 0.03). Those variables were not changed by amlodipine. The plasma levels of leptin and insulin 120 min after a glucose load decreased after moxonidine administration 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. Amlodipine, however, did not modify those variables. This study showed a comparable reduction in blood pressure with both antihypertensive drugs. Moxonidine decreased sympathetic nervous activity, improved insulin resistance and reduced the plasma levels of leptin.

Effects of magnesium on blood pressure and intracellular ion levels of Brazilian hypertensive patients.

Fifteen patients with uncomplicated mild to moderate primary hypertension (7 males, 8 females, age range 36-65 years) were submitted to a double blind randomized crossover study, receiving MgO 3 times a day at a daily dose of 1.0 g (600 mg/day of magnesium) and placebo for a period of 6 weeks. This was to test the effects of oral magnesium supplementation on blood pressure and sodium, potassium, calcium and magnesium intraerythrocyte concentrations. Concomitantly, plasma renin activity and serum aldosterone was also measured. Oral magnesium reduced significantly the systolic (delta = -7.6 mmHg, P < 0.05); diastolic (delta = -3.8 mmHg, P < 0.01) and mean blood pressure (delta = -5.9 mmHg, P < 0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (delta = -0.55 mEq/l per cell, P < 0.01) and intraerythrocyte magnesium concentration was increased (delta = 1.20 mg/dl per cell, P < 0.01). The diminution of the blood pressure correlated positively with the reduction in intraerythrocyte sodium (r = 0.66, P < 0.01) after magnesium. However, our results have shown that the blood pressure response to oral magnesium was not homogeneous. Forty percent of our patients had their blood pressure effectively controlled (more than 10 mmHg reduction in mean blood pressure), being the hypotensive effect more evident in patients with recent hypertension and in those where the reduction in intraerythrocyte sodium was significantly greater than in the non-responder individuals. Intraerythrocyte potassium and calcium, serum aldosterone, plasma renin activity and urinary sodium excretion were maintained unchanged after magnesium supplementation. These data showed that oral magnesium supplementation may reduce the blood pressure, which can be partially explained by the decrease in intracellular sodium and augment in intracellular magnesium.

[The effect of urapidil on blood pressure, renal hemodynamics, lipid and glucose metabolism]. / Efeito do urapidil sobre a pressão arterial, hemodinâmica renal, metabolismo lipídico e glicídico.

PURPOSE: To evaluate the effects of urapidil on blood pressure (BP), renal hemodynamics and lipid and glucose metabolism, in patients with mild-to-moderate uncomplicated essential hypertension. METHODS: Fifteen hypertensive patients, aged 38-64 year-old were studied by ambulatory blood pressure monitoring system (ABPM). It was also evaluated: 1) the creatinine clearance; 2) the effective renal plasma flow by use of a single plasma sample after injection of orthoiodohippurate; 3) the serum triglycerides, cholesterol, and HDL-cholesterol; 4) blood levels of glucose and insulin. The urapidil dose ranged from 60 to 180 mg/day, according to the individual response. RESULTS: The values after four weeks washout-placebo and active treatment with urapidil showed: the systolic/diastolic BP was reduced from 157.7 +/- 6/108.0 +/- 2 on placebo to 140.4 +/- 4/97.3 +/- 3 mmHg (p < 0.05/p < 0.01) after urapidil, respectively, whereas heart rate was unchanged. The percentage of elevated systolic and diastolic BP values during 24h (BP load) was reduced from 60.9% to 54.4% and from 60.8% to 50.3%, respectively. Effective renal plasma flow, glomerular filtration rate, filtration fraction and renal vascular resistance were unaltered by treatment. Significant increase in HDL-cholesterol was observed (from 39.5 +/- 3.6 on placebo vs 49.2 +/- 4.8 mg/dl (p < 0.01) after urapidil. Total cholesterol, LDL-cholesterol and triglycerides levels were not modified with treatment. Circulating plasma glucose and insulin remained unchanged. CONCLUSION: Urapidil is an effective antihypertensive agent without deleterious effect on renal hemodynamics, lipid and glucose metabolism.