1. The fall in renal sodium excretion after dietary sodium restriction is prompt and reproducible. The importance of increased aldosterone secretion during the early phase (within 48 h) of this response is unclear. Using two indirect measures of aldosterone secretion (in urine and saliva), we have tried to relate changes in excretion and concentration of this hormone to renal sodium excretion during the abrupt transition from a normal (approximately 150 mmol/day) or high (260 mmol/day) to a low (5–25 mmol/day) sodium intake in 11 and seven male volunteers, respectively.
2. All subjects showed reduced renal sodium excretion within 36 h of dietary restriction, but the times at which increases in renal aldosterone excretion, saliva aldosterone concentration and plasma renin activity became statistically significant varied widely (8–72 h, 2.5–>62.5 h and 38 h for renal aldosterone secretion, saliva aldosterone concentration and plasma renin activity, respectively). Circadian fluctuations in saliva aldosterone concentration were apparent and increased in amplitude during sodium restriction.
3. Urine flow rate tended to increase on the first day of sodium restriction and this reached statistical significance in the group initially on a high sodium intake (64.0 ± 8.8 to 84.3 ± 11.2 ml/h, P <0.01); although the pattern of urine flow did correlate with plasma arginine vasopressin concentration (r = −0.49, P <0.01), there was no significant decrease in mean plasma arginine vasopressin concentration [1.15 (0.92–1.44) to 0.90 (0.72–1.12) pmol/l, P = 0.08; geometric mean and 95% confidence limits]. Renal arginine vasopressin excretion fell significantly after the change from a normal or high to a low sodium diet [2.70 (2.38–8.69) to 2.19 (1.72–4.00) and 3.80 (2.92–5.01) to 2.50 (1.26–2.35) pmol/h, respectively, P <0.05]; in four subjects assayed, plasma atrial natriuretic peptide concentration also fell significantly [20.1 (16.3–24.9)to 13.1 (10.6–16.2) pmol/l, P <0.05].
4. We conclude that after acute dietary sodium withdrawal: (1) unless enhanced renal sensitivity to aldosterone develops rapidly, increased secretion alone is unlikely to account for the initial decline in renal sodium excretion; (2) decreased atrial natriuretic peptide secretion may have a permissive role in ‘low-sodium’ adaptation; (3) the early ‘low-sodium’ diuresis is probably vasopressin-dependent and is an important mechanism in the preservation of normal plasma osmolality.