Responses to acute sodium loading depend on the load and on level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03-0.75mmol/kg/d for 7 days. Acute NaCl administration increased PV (+6.3-8.9%) and plasma sodium concentration (~2%) and decreased plasma protein concentration (-6.4-8.1%). Plasma angiotensin II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms which are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down regulated within 2 hrs. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines which are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma angiotensin II concentration increases from theoretical zero at a daily sodium intake of 17mmol Na/kg (intercept) with a slope of 16pM increase per decade of decrease in dietary sodium intake.