We showed previously that a single dose of ethanol acts as a stressor in female rats (Milovanovic et al., 2003). In order to extend this observation, we investigated whether the effect of ethanol on ACTH is dose-related and possible interactions between nitric oxide (NO) and alcohol on the level of ACTH. To this end, adult female Wistar rats showing diestrus day 1 were treated with: (a) ethanol (2 or 4 g/kg, i.p.), (b) Nω-nitro-L-arginine-methyl ester (L-NAME), which blocks the activity of all isoforms of nitric oxide synthase, (30 mg or 50 mg/kg, s.c.) followed by ethanol (2 or 4 g/kg, i.p.) 3 h later and (c) L-NAME (30 mg or 50 mg/kg, s.c.) followed by saline 3 h later. Untreated rats were used as controls. The animals were sacrificed 0.5 h after ethanol administration. Blood ethanol levels were measured using gas chromatography. Plasma concentrations of ACTH were determined by radioimmunoassay. Obtained results showed that acute ethanol treatment significantly, dose-relatedly, enhanced the level of ACTH (P<0.01). The same phenomenon was observed in the groups treated with different doses of L-NAME followed by ethanol (P<0.05). Elevated concentration of ACTH was also found in the groups injected with L-NAME followed by saline (P<0.05).
Our results suggest that acute ethanol treatment increases the level of ACTH in dose-dependent manner. Although endogenous NO exerts negative influence on ACTH, it seems that it is not involved in the observed effect of ethanol under these experimental conditions.
Milovanovic T. et al. J Stud Alcohol 64:662668, 2003.
(Supported by grant 145087 from the Ministry of Science of Serbia)