Release of aldosterone and corticosterone from the adrenal cortex of the Brattleboro rat in response to administration of ACTH.
The time-course and dose-response of the in-vivo secretion of aldosterone and corticosterone after administration of ACTH(1-24) were measured in adrenal venous blood from female Brattleboro rats, homozygous for hypothalamic diabetes insipidus and lacking arginine vasopressin (AVP). Female Long-Evans rats were used as controls. All animals were pretreated with dexamethasone and anaesthetized with pentobarbital. Basal secretions of aldosterone and corticosterone were four- to sixfold lower in Brattleboro than in Long-Evans rats. Administration of ACTH consistently increased the secretion of aldosterone and corticosterone similarly in the two groups of rats; maximum values were observed 20-30 min after ACTH injection. However, for all the doses of ACTH (0.05, 0.5 and 5.0 mi.u./100 g body wt) and at every stage of response the secretion rates of aldosterone and corticosterone were twofold lower in Brattleboro than in Long-Evans rats. Furthermore the absolute increase in steroid secretion induced by ACTH was reduced by half in Brattleboro rats. These results show that the impairment of adrenal activity is largely due to a reduced capacity for corticosteroidogenesis in the adrenal cortex of Brattleboro rats. The mechanisms of action of AVP are discussed.
D000302:Adrenal Cortex / Q000187:drug effects*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000450:Aldosterone / Q000097:blood*; D000818:Animals; D001127:Arginine Vasopressin / Q000172:deficiency; D003345:Corticosterone / Q000097:blood*; D003366:Cosyntropin / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D051381:Rats; D011910:Rats, Brattleboro / Q000502:physiology*; D011922:Rats, Mutant Strains / Q000502:physiology*
D001127:Arginine Vasopressin; D003366:Cosyntropin; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone