Isotonic and hypertonic sodium loading in supine humans

The hypothesis that hypertonic saline infusion induces a greater natriuresi s than infusion of the same amount of sodium as isotonic saline was tested in 8 supine subjects on fixed sodium intake of 150 mmol NaCl day(-1). Sodiu m loads equivalent to the amount of sodium contained in 10% of measured ext racellular volume were administered intravenously over 90 min either as iso tonic saline or as hypertonic saline (850 mmol L-1). A third series without saline infusion served as time control. Experiments lasted 8 h. Water bala nce and sodium loads were maintained by replacing the excreted amounts ever y hour. Plasma sodium concentrations only increased following hypertonic sa line infusion (by 2.7 +/- 0.3 mmol L-1). Oncotic pressure decreased signifi cantly more with isotonic saline (4.1 +/- 0.3 mmHg) than with hypertonic sa line (3.2 +/- 0.2 mmHg), indicating that isotonic saline induced a stronger volumetric stimulus. Renal sodium excretion increased more than a factor o f four with isotonic and hypertonic saline but also increased during time c ontrol (factor of three). Cumulated sodium excretions following isotonic (1 31 +/- 13 mmol) and hypertonic saline (123 +/- 10 mmol) were statistically identical exceeding that of time control (81 +/- 9 mmol). Plasma angiotensi n II decreased in all series but plasma ANP concentrations and urinary excr etion rates of endothelin-1 remained unchanged. In conclusion, hypertonic s aline did not produce excess natriuresis. However, as the two loading proce dures induced similar natriureses during different volumetric stimuli, part of the natriuresis elicited by hypertonic saline could be mediated by stim ulation of osmoreceptors involved in renal sodium excretion. The supine pos ition does not provide stable time control conditions with regard to renal excretory function.