Evidence is presented that the retention of sodium observed during development is consequent primarily to enhanced tubular reabsorption rather than to low rates of glomerular filtration. The enhanced transport of sodium occurs in nephron segments located beyond the proximal tubule, apparently under the stimulation of the high plasma concentration of aldosterone. This adaptive mechanism may account for the fact that the infant thrives on a rather low intake of sodium, as prevails during the period of breast-feeding. The renin-angiotensin-aldosterone system cannot be fully inhibited even by intravascular volume expansion and this may account for the blunted natriuretic response of the developing animal and human to the acute infusion of saline or albumin solutions. Conversely, the renal sodium loss and the hyponatremia often encountered in premature babies appear to be due to an insufficient rise in aldosterone secretion or to a limited responsiveness of the distal tubule to aldosterone stimulation.