title: Hypoglycemia stimulates ACTH secretion through a direct effect on the basal hypothalamus.
abstract: 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.
mesh_terms: 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
chemical_list: D001786:Blood Glucose; D007328:Insulin; D009020:Morphine; D000324:Adrenocorticotropic Hormone; D010424:Pentobarbital; D002746:Chlorpromazine; D003345:Corticosterone