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Conscious trained sheep with adrenal autotransplants and a unilateral parotid fistula were studied. Progressive depletion of sodium, up to 900 mEq. over 69 h, resulted in a progressive and proportional increase in aldosterone secretion rate, the peripheral blood concentration of aldosterone and angiotensin, and the plasma renin level. The same parameters were then studied following the rapid correction of sodium depletion by voluntary drinking of 2–3 1 of hypertonic NaHCO3 solution (300 mEq./l). In 11 of 12 experiments, where animals rapidly drank adequate sodium solution to correct body deficit, aldosterone secretion fell close to, or into the sodium replete range within 6 h after drinking. Although plasma renin concentration and blood angiotensin levels also tended to decrease, they fell at a much slower rate than the aldosterone secretion rate. The dissociation was most apparent about two hours after drinking NaHCO3 solution. On occasions, large fall of aldosterone occurred without fall of angiotensin. However, the close correlation between renin and angiotensin was unchanged. The results were indicative that, during rapid correction of sodium deficiency, aldosterone secretion rate was determined by factors other than, or additional to, the contemporary level of angiotensin in peripheral blood. The question whether changes in plasma ionic concentrations could wholly, or only partly account for this disjunction between angiotensin and aldosterone is discussed, and the existence of an aldosterone inhibitory mechanism is postulated.