RESUMEN
AIMS: In vasopressin-deficient rat pups stressor-induced adrenocorticotropin (ACTH) and corticosterone elevations markedly dissociate. We have shown recently that during the postnatal period mineralocorticoid secretion is more sensitive to stressor exposure than that of glucocorticoids. We have therefore hypothesized that in vasopressin-deficient pups during hypoglycemia, a stressor triggering aldosterone release mainly via ACTH, aldosterone release will change in parallel with ACTH. An additional aim was to reveal at which stage of the development occurs the shift from aldosterone to corticosterone as primarily stressor-induced adrenocortical hormone. MAIN METHODS: Vasopressin-deficient (di/di) and control Brattleboro rats were used both postnatally (10-day-old rats) and in adulthood. KEY FINDINGS: Hypoglycemia induced similar ACTH elevations in pups and adults with significantly lower levels in di/di rats. In contrast, vasopressin-deficiency resulted in elevated resting aldosterone and stressor-induced corticosterone levels in pups without genotype differences in adults. Thus, aldosterone levels also dissociated from ACTH secretion. During stress, pups showed only minimal corticosterone increase, with relatively high aldosterone elevation. Resting levels of gluco- and mineralocorticoid receptor mRNA were smaller, while corticosterone-deactivating enzyme (11ß-HSD2) mRNA level were higher in the hippocampus of 10-day-old rats compared to adults. SIGNIFICANCE: AVP does not seem to substantially regulate the stressor-induced aldosterone production, but both hormones contribute to salt-water regulation. Postnatally higher stressor-induced aldosterone than corticosterone production was still detectable in 40-day-old rats, although to a lesser extent, supporting a shift in the balance between stressor-induced glucocorticoid and mineralocorticoid hormone release throughout the development occurring in rats after postnatal day 40.
