ADRENOCORTICAL FUNCTION IN NEONATAL AND WEANLING BEAGLE PUPS

Adrenocortical function was assessed in 27 Beagle pups at 2, 4, 6, 8, 10, and 12 weeks of age by determination of plasma sodium, potassium, and chloride concentrations; serum aldosterone and cortisol concentrat ions; and plasma ACTH concentrations. Serum cortisol concentration was measured before and 1 and 2 hours after IM administration of 2.2 IU o f ACTH/kg of body weight. Serum progesterone concentration also was de termined for all pups at 2, 4, and 6 weeks of age. Mean baseline corti sol concentration was lower for pups 8 weeks old or younger than for m ature dogs. Nevertheless, mean serum ACTH-stimulated cortisol concentr ation in dogs of all age groups increased into the adult reference ran ge after administration of ACTH. For pups 4 weeks old or younger, incr ease in cortisol concentration was maximal at 2 hours after ACTH admin istration. However, in pups between 6 and 12 weeks of age, the increas e in cortisol concentration was maximal 1 hour after ACTH administrati on in about a third of the pups, whereas the remaining pups had peak v alues at 2 hours. Mean plasma sodium, potassium, and chloride concentr ations for each age group were within the reference ranges established for mature dogs, with the exception of lower mean plasma sodium and c hloride concentrations in pups 4 weeks old or younger. Mean serum aldo sterone concentration in pups of each age group was substantially high er than the range of aldosterone concentrations for clinically normal mature dogs. Median progesterone concentration was uniformly less than 0.2 ng/ml for all pups 6 weeks old or younger. The normal endogenous ACTH concentration and adequate cortisol responses to exogenous ACTH s een in our pups would support functional pituitary gland and adrenal c ortex for cortisol production. The low baseline cortisol concentration observed in the pups of this study may be related to reduced binding of cortisol to plasma proteins, as exists in human infants. The hypona tremia and increased aldosterone concentration may be explained by red uced renal tubular response to aldosterone, as also evidenced in the h uman infant kidney.