The Hypothalamus and Pituitary ACTH Release

Abstract

Normal pituitary adrenocorticotropic activity is dependent upon the hypothalamus and the hypophyseal portal blood vessels, which carry transmitter substances from the median eminence (ME) to the gland. The basal level of ACTH secretion may be independent of hypothalamic activity and may be controlled by corticosteroids in the blood. The mechanisms controlling ACTH release under non-stress and stress conditions are functionally dissociable because small doses of corticosteroids suppress the marked circadian rise in plasma corticosterone without affecting the stress response. A considerable amount of evidence has been found to suggest that corticotropin releasing factor (CRF) may be identical to vasopressin. Thus, rats in which the stress-induced release of ACTH has been abolished by hypothalamic lesions also exhibit diabetes insipidus and the release of ACTH can be elicited in these animals by vasopressin injections.