Resumo

Although the rise of corticosterone (Cort) secretion is the main marker of stress responses, stress also increases progesterone (P) levels. We studied how P and testosterone (T) responded to restraint in rats, and the role of gonadal steroids on this response. Males rats, intact treated with oil (INT) or RU486 (RU), castrated treated with oil (ORQ) or testosterone (ORQT) and female on proestrous, castrated treated with oil (OVO) or estrogen (OVE) rats underwent jugular cannulation. On the next morning, blood samples were collected at -5, 15, 30, 45, 60 (restraint from 0-60 min), 90 and 120 min. Plasma P, T, DHEA, LH and Cort were measured. In male rats, stress induced an acute and robust rise in P and lowered T levels, which were not blocked by RU. Castration blunted P rise and T replacement did not revert this effect. Stress increased Cort in all groups but ORQT. LH levels did not change in any group. In females, stress induced P and Cort rise in all groups, but estrogen treatment blunted Cort rise. Stress increased LH in OVE rats but did not change DHEA in any group. P is a good marker of stress response since it is similar to that of Cort. Adrenal seems to be the only P source in stressed females while in stressed males P seems to come also from testis. P and T response to stress do not depend on LH and the decrease of T seems not to be mediated by Cort in the testis. Gonadal steroids inhibit Cort responses in both genders. Financial support: FAPESP and CNPq