Corticotropin-releasing factor: a physiologic regulator of adrenal epinephrine secretion.
Pituitary adrenocorticotropic hormone (ACTH) secretion following stress is mediated primarily by the release of corticotropin-releasing factor (CRF) from the brain. We have hypothesized that stress-induced alterations of autonomic nervous system activity also may be dependent on CRF release within the brain because administration of CRF into the brain produces changes in autonomic nervous system function that are similar to those observed following exposure to various types of stress. We now report confirmation of this hypothesis with studies using a CRF receptor antagonist. The CRF receptor antagonist, alpha-helical CRF9-41, placed into the brains of rats suppressed stress-induced elevations of plasma epinephrine levels. Thus, CRF appears to be physiologically involved in coordinating the pituitary and autonomic nervous system responses to stress.
D000313:Adrenal Medulla / Q000378:metabolism*; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D001786:Blood Glucose / Q000032:analysis; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology / Q000502:physiology*; D004837:Epinephrine / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013312:Stress, Physiological / Q000503:physiopathology*
D001786:Blood Glucose; D010446:Peptide Fragments; D003346:Corticotropin-Releasing Hormone; C045089:corticotropin releasing hormone (9-41); D009638:Norepinephrine; D004837:Epinephrine