Nitric oxide mediates the interleukin-1beta- and nicotine induced hypothalamic-pituitary-adrenocortical response during social stress

• Autorzy: Gadek-Michalska A. , Bugajski J.
• Języki publikacji: EN

Abstrakty

EN

We investigated the role of nitric oxide (NO) in the interleukin 1b (IL-1ß) and nicotine induced hypothalamic-pituitary-adrenal axis (HPA) responses, and a possible significance of CRH and vasopressin in these responses under basal and social stress conditions. Male Wistar rats were crowded in cages for 7 days prior to treatment. All compounds were injected i.p., nitric oxide synthase (NOS) inhibitors, a-helical CRH antagonist and vasopressin receptor antagonist 15 min before IL-1ß or nicotine. Identical treatment received control non-stressed rats. Plasma ACTH and serum corticosterone levels were measured 1 h after IL-1ß or nicotine injection. L-NAME (2 mg/kg), a general nitric oxide synthase (NOS) inhibitor, considerably reduced the ACTH and corticosterone response to IL-1ß (0.5 µg/rat) the same extent in control and crowded rats. CRH antagonist almost abolished the nicotine-induced hormone responses and vasopressin antagonist reduced ACTH secretion. Constitutive endothelial eNOS and neuronal nNOS inhibitors substantially enhanced the nicotine-elicited ACTH and corticosterone response and inducible iNOS inhibitor, aminoguanidine, did not affect these responses in non-stressed rats. Social stress significantly attenuated the nicotine-induced ACTH and corticosterone response. In crowded rats L-NAME significantly deepened the stress-induced decrease in the nicotine-evoked ACTH and corticosterone response. In stressed rats neuronal NOS antagonist did not alter the nicotine-evoked hormone responses and inducible NOS inhibitor partly reversed the stress-induced decrease in ACTH response to nicotine. These results indicate that NO plays crucial role in the IL-1ß-induced HPA axis stimulation under basal and social stress conditions. CRH and vasopressin of the hypothalamic paraventricular nucleus may be involved in the nicotine induced alterations of HPA axis activity. NO generated by eNOS, but not nNOS, is involved in the stress-induced alterations of HPA axis activity by nicotine.

Słowa kluczowe

EN

interleukin 1beta; male; nitric oxide; corticosterone; nicotine; hypothalamic-pituitary-adrenocortical response; social stress; rat; stress condition; hypothalamic-pituitary-adrenal axis

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2005
• Tom: 56
• Numer: 3
• Opis fizyczny: p.491-503,fig.,ref.

Twórcy

autor

Gadek-Michalska A.

• Polish Academy of Sciences, 12 Smetna Street, 31-343 Krakow, Poland

autor

Bugajski J.