Social stress inhibits the nitric oxide effect on the corticotropin-releasing hormone- but not vasopressin-induced pituitary–adrenocortical responsiveness

• Published in: Brain research 1999-01, Vol.817 (1-2), p.220-225
• Main Authors: Bugajski, Jan, Gądek-Michalska, Anna, Borycz, Janusz, Głód, Radosław
• Format: Article
• Language: English
• Subjects: ACTH/Corticosterone; Animals; Arginine Vasopressin - metabolism; Behavioral psychophysiology; Biological and medical sciences; Corticotropin-releasing hormone; Corticotropin-Releasing Hormone - metabolism; Enzyme Inhibitors - pharmacology; Fundamental and applied biological sciences. Psychology; Hormones and behavior; Male; Nitric oxide; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; Nitroarginine - pharmacology; Pituitary-Adrenal System - physiology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rats; Rats, Wistar; Secretory Rate; Social Environment; Social stress; Stress, Psychological - physiopathology; Vasopressin
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(98)01209-8

Putative involvement of endogenous nitric oxide (NO) in the corticotropin-releasing hormone (CRH, 1 μg/kg i.p.)- and vasopressin (AVP, 5 μg/kg i.p.)-induced ACTH and corticosterone secretion was investigated in both non-stressed and crowded rats. The NO synthase blocker Nω-nitro-l-arginine (l-NNA, 2 mg/kg i.p.) significantly augmented the AVP-induced ACTH and corticosterone secretion in control and stressed rats, but it increased the CRH-induced ACTH response only in control rats. Crowding stress did not affect the l-NNA evoked increase in AVP-induced hormone responses, but it abolished the CRH-induced ACTH response.