Modulation of stress-induced ACTH release by corticotropin-releasing factor, catecholamines and vasopressin.
The stress-induced release of ACTH is believed to involve the activation of several humoral and neural pathways, including corticotropin-releasing factor (CRF), catecholamines and vasopressin. The essential role of CRF was supported by our observation that immunoneutralization of this releasing factor significantly lowers plasma ACTH levels of ether-stressed rats. However, the presence of a small but measurable residual ACTH secretion suggested the possible involvement of factors other than CRF in the stress response. We report here that pretreatment with a vasopressin antagonist decreases the plasma ACTH levels of ether-stressed rats in later (10-20 min), but not earlier (0-10 min), phases of ether stress. The ganglionic blocker chlorisondamine, inhibits ACTH release during both phases of the response to ether by 40-60% when used alone, and by 100% when administered with anti-CRF antibody. These results support a role of CRF, catecholamines and vasopressin in mediating ACTH release by ether stress.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D000937:Antigen-Antibody Reactions; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology*; D002714:Chlorisondamine / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000502:physiology*; D051381:Rats; D012636:Secretory Rate / Q000187:drug effects; D013312:Stress, Physiological / Q000503:physiopathology*; D014667:Vasopressins / Q000502:physiology*
D002395:Catecholamines; D014667:Vasopressins; D001127:Arginine Vasopressin; C028888:argipressin, deaminopenicillamine(1)-O-methyl-Tyr(2)-; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D002714:Chlorisondamine