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Ten obese men (20-40% overweight) with previously untreated arterial hypertension (WHO stages I and II) were examined before and during sodium-restricted isocaloric diets. The mean (± s.d.) daily sodium excretion was reduced from 199 ± 65 to 65 ± 25 mmol/24 h. Intra-arterial blood pressure (BP), cardiac output (CO), plasma volume, circulating and urinary noradrenaline (NA), plasma renin activity (PRA) and urinary aldosterone were measured. Vascular reactivity was assessed with intravenous bolus injections of 50, 100 and 200 µg phenylephrine, and baroreflex sensitivity was assessed with the R-R interval response to pressure elevations on electrocardiogram.Significant reductions in systolic BP from 163 ± 18 to 147 ± 17 mmHg and in diastolic BP from 97 ± 7 to 88 ± 9 mmHg occurred during salt restriction. Blood pressure reductions were correlated with changes of urinary sodium excretion (r=0.71; P<0.05). No significant changes in CO, heart rate (HR) or stroke volume (SV) were observed; therefore, BP reduction was secondary to the fall in total peripheral resistance (TPR) from 21.8 ± 4.1 to 19.0 ± 4.1 units (P=0.05). Plasma volume, as well as total blood volume, was not affected by the moderate sodium restriction, but PRA rose from 0.71 ± 0.1 to 0.87 ± 0.1 µg angiotensin l/ml per h (P<0.05). Urinary aldosterone was increased from 32 ± 12 to 54 ± 9 nmol/24 h. No change in venous or arterial concentrations of NA or of urinary NA was observed. However, there was an increased pressure response to phenylephrine injections. Baroreceptor sensitivity was unchanged. In conclusion, sodium restriction with isocaloric energy intake caused a BP reduction which was related significantly to the degree of sodium restriction, and which was characterized by unchanged cardiac index and reduced resting TPR. This haemodynamic profile contrasts with the reduced HR and CO the authors found in matched patients on combined sodium and calorie restriction.