The hypothesis was tested that cardiac output (CO) and stroke volume (SV) are increased by a moderate physiological elevation in sodium intake with a more pronounced effect in the ambulatory upright seated than supine position. Fourteen healthy males were investigated during ambulatory and controlled laboratory conditions at the end of two consecutive 5-day periods with sodium intakes of 70 (low) and 250 (high) mmol/24-h or vice versa, respectively. Comparing high and low sodium intake, plasma volume and plasma protein concentrations were 9 and 8% higher in the seated and the supine position, respectively. When seated during laboratory conditions, CO was 5.3 ±0.2 l/min on the high sodium intake vs. 4.8 ±0.2 l/min on the low (p<0.05), and SV was 81 ±3 ml vs.68 ±3 ml (p<0.05). In the supine position, SV was 107 ±3 ml on the high vs. 99 ±3 ml (p<0.05) on the low sodium intake, while CO remained unchanged. The difference in CO and SV induced by the change in sodium intake was significantly higher in the seated than in the supine position (p<0.05). During upright ambulatory conditions, CO was 5.9 ±0.2 l/min during the high and 5.2 ±0.2 l/min during the low sodium intake (p<0.05), and SV was 84 ±3 and 69 ±3 ml (p<0.05) respectively. Mean arterial pressure was unchanged by the variations in sodium intake. In conclusion, increments in sodium intake within the normal physiological range increase CO and SV and more so in the seated vs. the supine position. These changes are readily detectable during upright, ambulatory conditions. The results indicate that the higher SV and CO could constitute an arterial baroreflex stimulus for the augmented renal sodium excretion.