Hypoglycemia stimulates ACTH secretion through a direct effect on the basal hypothalamus.
The primary site of action of insulin hypoglycemia to induce ACTH secretion was investigated in rats with medial basal hypothalamic ablation (MBHA), medial basal hypothalamic deafferentation (MBHD), and chlorpromazine-morphine-pentobarbital (C-M-P) treatment. Plasma corticosterone (B) concentration was used as an index of ACTH secretion. Hypoglycemia failed to provoke ACTH secretion in MBHA and C-M-P treated animals, while it stimulated ACTH secretion in MBHD animals to the same extent as in controls. The rise in plasma B induced by synthetic lysine-vasopressin injection was not significantly different between MBHA and control animals, indicating pituitary ACTH reserve was not affected by the operation. Our data indicate that hypoglycemia stimulates ACTH secretion through a primary effect in the medial basal hypothalamus and not in the extrahypothalamic CNS or adenohyphophysis.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000503:physiopathology; D002746:Chlorpromazine / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood; D007003:Hypoglycemia / Q000139:chemically induced / Q000503:physiopathology*; D007031:Hypothalamus / Q000502:physiology / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009020:Morphine / Q000494:pharmacology; D010424:Pentobarbital / Q000494:pharmacology; D010902:Pituitary Gland / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D007328:Insulin; D009020:Morphine; D000324:Adrenocorticotropic Hormone; D010424:Pentobarbital; D002746:Chlorpromazine; D003345:Corticosterone