Immature chickens and ducks were maintained on synthetic diets containing normal (0.4%), low (0.018%), or high (1.9%) sodium for 8 days, with freshwater available ad libitum. Food intake was similar in both species regardless of the diet but weight gain was depressed in birds fed the low-sodium diet. In both species the circulating aldosterone concentration was increased within 24 hr of dietary sodium depletion, although maximal levels were not attained until after 5 days. The magnitude of adrenocorticotrophin (ACTH)-induced aldosterone secretion was also increased in sodium-deprived chickens and ducks. The basal aldosterone level was slightly suppressed by excess dietary sodium, which blunted the aldosterone response to exogenous ACTH. The transfer of chickens and ducks from low- to high-sodium regimes reduced the aldosterone levels (within 24 hr) to those in their respective controls. The transfer of birds from high- to low-sodium diets resulted in a prompt increase in the aldosterone concentration, although of reduced magnitude when compared with control birds transferred to low sodium. In both species alterations in the dietary sodium content had no effect on basal or ACTH-induced corticosterone secretion. The plasma prolactin levels in chickens were also unrelated to their sodium status. These results suggest that homeostatic adaptations in electrolyte balance during sodium depletion or excess are principally mediated by alterations in aldosterone secretion.

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