On the hypotensive response to weight reduction : cardiovascular regulation during dietary energy and sodium restriction in obese men with mild primary hypertension / Björn Fagerberg.

Por: Fagerberg, BjörnDetalhes da publicação: Göteborg [s.n.] 1984Notas: 99 fAssunto(s): Peso corporal | Hipertensão -- Terapêutica | Obesidade -- DietoterapiaClassificação Decimal de Dewey: 616.132 Nota de dissertação: Tese (doutor) - University of Göteborg, 1984 Sumário: Thirty middle-aged men with 20-40% overweight and untreated mild prima hypertension (diastolic blood pressure 95-105 mm Hg) were randomized to two groups comparable with regard to heredity for hypertension, age, body mass, body fat, mean cell size, plasma renin activity, and 24-hour sodium and noradrenaline excretion. During baseline period of 4 to 6 weeks the patients continued with their habitual diet. In the ensuing diet period (9 to 11 weeks) energy intake was restricted to about 5.1 MJ (1200 kcal) both groups. In Group I (n=15) sodium chloride supplementation was given to maintain the sodium intake at the prediet level. In Group II (n=15) sodium intake was restricted. This study was ambulatory. The patients met regularly with a doctor and a dietitian who monitored the diet with diet histories and sodium excretion data from four 24-h urine samples. The groups showed comparable decreases in body mass (8.6 kg (SE 0.6) and 8.2 kg (SE 0.7) respectively). Measurements of the urinary sodium excretion indicated that Group I had an unchanged sodium intake while Group II decreased mean 24-h sodium excretion with 81 mmol/24 h. Studies of the body composition in Group II, using determinations of 40K and tritiated water, showed that sodium and energy restriction was accompanied by decreases of body fat, body cell mass and intracellular water while the extracellular water compartment expanded. Plasma volume was unchanged. The blood pressure was significantly reduced only during dieting with both sodium and energy restriction. Auscultatory and intra-arterial blood pressure fell (Group II) as did heart rate and cardiac output (dye-dilution technique) while total peripheral resistance was unchanged. These alterations are suggestive of a lowered adrenergic activity. In Group I there were no significant hemodynamic changes except for a reduction in heart rate. 24-h urinary noradrenaline excretion decreased in both groups. Noradrenaline levels in arterial plasma fell in Group II while mixed venous plasma content showed no significant changes in either group. Group I (n=10) had an increased pressor response to noradrenaline infusion during the energy restricted diet. Concomitant sodium and energy restriction in Group II (n=8) was not associated with any change in cardiovascular reactivity. These findings indicate that a moderately low energy diet decreases sympathetic nervous activity. However, blood pressure did not fall since the expected hypotensive effect of diminished neural outflow was offset by a concomitant up-regulation of the vascular reactivity (Group I). When energy restriction was combined with reduction of sodium intake, then this up-regulation did not occur, and the decreased sympathetic outflow lowered blood pressure(Group II). There were no indications that diet induced changes in cardiovascular regulation were caused by alterations in renin, aldosterone, insulin or triiodothyronine.
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Tese T 616.132 F153o (Percorrer estante(Abre abaixo)) Disponível 01-0283

Tese (doutor) - University of Göteborg, 1984

Thirty middle-aged men with 20-40% overweight and untreated mild prima hypertension (diastolic blood pressure 95-105 mm Hg) were randomized to two groups comparable with regard to heredity for hypertension, age, body mass, body fat, mean cell size, plasma renin activity, and 24-hour sodium and noradrenaline excretion. During baseline period of 4 to 6 weeks the patients continued with their habitual diet. In the ensuing diet period (9 to 11 weeks) energy intake was restricted to about 5.1 MJ (1200 kcal) both groups. In Group I (n=15) sodium chloride supplementation was given to maintain the sodium intake at the prediet level. In Group II (n=15) sodium intake was restricted. This study was ambulatory. The patients met regularly with a doctor and a dietitian who monitored the diet with diet histories and sodium excretion data from four 24-h urine samples. The groups showed comparable decreases in body mass (8.6 kg (SE 0.6) and 8.2 kg (SE 0.7) respectively). Measurements of the urinary sodium excretion indicated that Group I had an unchanged sodium intake while Group II decreased mean 24-h sodium excretion with 81 mmol/24 h. Studies of the body composition in Group II, using determinations of 40K and tritiated water, showed that sodium and energy restriction was accompanied by decreases of body fat, body cell mass and intracellular water while the extracellular water compartment expanded. Plasma volume was unchanged. The blood pressure was significantly reduced only during dieting with both sodium and energy restriction. Auscultatory and intra-arterial blood pressure fell (Group II) as did heart rate and cardiac output (dye-dilution technique) while total peripheral resistance was unchanged. These alterations are suggestive of a lowered adrenergic activity. In Group I there were no significant hemodynamic changes except for a reduction in heart rate. 24-h urinary noradrenaline excretion decreased in both groups. Noradrenaline levels in arterial plasma fell in Group II while mixed venous plasma content showed no significant changes in either group. Group I (n=10) had an increased pressor response to noradrenaline infusion during the energy restricted diet. Concomitant sodium and energy restriction in Group II (n=8) was not associated with any change in cardiovascular reactivity. These findings indicate that a moderately low energy diet decreases sympathetic nervous activity. However, blood pressure did not fall since the expected hypotensive effect of diminished neural outflow was offset by a concomitant up-regulation of the vascular reactivity (Group I). When energy restriction was combined with reduction of sodium intake, then this up-regulation did not occur, and the decreased sympathetic outflow lowered blood pressure(Group II). There were no indications that diet induced changes in cardiovascular regulation were caused by alterations in renin, aldosterone, insulin or triiodothyronine.

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