Osmoregulatory control of renal sodium excretion after sodium loading in humans

The hypothesis that renal sodium handling is controlled by changes in plasm a sodium concentration was tested in seated volunteers. A standard salt loa d (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot ) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa (+)) or 300 mmol/day (HiNa(+)). Hypr increased plasma sodium by similar to 4 mmol/l but increased plasma volume and central venous pressure significan tly less than Isot irrespective of diet. After LoNa(+), Hypr induced a smal ler increase in sodium excretion than Isot (48 +/- 8 vs. 110 +/- 17 mu mol/ min). However, after HiNa(+) the corresponding natriureses were identical ( 135 +/- 33 vs. 139 +/- 39 mu mol/min), despite significant difference betwe en the increases in central venous pressure. Decreases in plasma ANG II con centrations of 23-52% were inversely related to sodium excretion. Mean arte rial pressure, plasma oxytocin and atrial natriuretic peptide concentration s, and urinary excretion rates of endothelin-1 and urodilatin remained unch anged. The results indicate that an increase in plasma sodium may contribut e to the natriuresis of salt loading when salt intake is high, supporting t he hypothesis that osmostimulated natriuresis is dependent on sodium balanc e in normal seated humans.