title: Effect of cyclooxygenase inhibitors on the vasopressin induced ACTH and corticosterone response during crowding stress.
abstract: The aim of the present study was to compare the effect of social stress on the corticotropin releasing hormone (CRH) and arginine vasopressin (AVP)-induced pituitary-adrenocortical activity. Also the significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by AVP under basal and crowding stress conditions was investigated. The control rats were housed 7 in a standard cage and stressed rats were crowded 24 in a cage of the same size during 7 days. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. AVP administration. Indomethacin (2.0 mg/kg i.p.), a non-selective COX inhibitor, piroxicam (0.2, 2.0, and 5.0 mg/kg), a more potent COX-1 than COX-2 inhibitor, and compound NS-398 (0.2 and 2.0 mg/kg) a selective COX-2 inhibitor, were administered i.p. 15 min prior to AVP (5.0 microg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 7 days considerably inhibits the stimulatory action of AVP on ACTH secretion, while it intensifies the CRH-induced ACTH secretion. Indomethacin, piroxicam and NS-398 significantly diminished the AVP-elicited ACTH and corticosterone secretion in non-stressed rats. None of these COX antagonist induced any significant inhibition of the AVP-induced ACTH and corticosterone secretion in stressed rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the HPA stimulation by AVP during crowding stress. These results suggest that social crowding stress desensitizes the PG stimulatory mechanism which considerably mediates the AVP-induced HPA stimulation under basal conditions. The results contrast with a lack of any involvement of PG in the CRH-induced stimulation of HPA response under basal or crowding stress conditions.
authors.affiliation: Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences, Cracow, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Bugajski
authors.forename: A
authors.initials: A
authors.lastname: Gadek-Michalska
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood* / Q000378:metabolism; D000818:Animals; D003345:Corticosterone / Q000097:blood* / Q000378:metabolism; D003441:Crowding / Q000523:psychology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013315:Stress, Psychological / Q000097:blood* / Q000201:enzymology; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D014667:Vasopressins; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone