The present study investigates the acute consequences of central adrenergic stimulation on the release of steroids from the ovary. The influence of the superior ovarian nerve (SON) and the relationship between the neural effect and peripheral LH levels were also examined.The intracerebroventricular (i.c.v.) injection of 5 µg epinephrine in SON-intact rats on day 1 of dioestrus (D1) increased progesterone levels in ovarian vein blood from 7 to 21 min after injection but the same injection in SON-intact rats on day 2 of dioestrus (D2) decreased progesterone levels in ovarian vein blood from 1 to 25 min. A smaller dose (0·5 µg) of epinephrine injected i.c.v. in SON-intact rats produced a decrease in progesterone levels in ovarian vein blood of shorter duration. In SON-transected (SONt) animals, 0·5 µg epinephrine i.c.v. caused a smaller decrease in progesterone levels compared with SON-intact rats (P<0·05). On the other hand, in SON-intact rats on D2, the i.c.v. injection of 0·5 µg epinephrine did not modify the peripheral LH levels during 25 min, but 5 µg epinephrine injected i.c.v. raised the peripheral LH level from the third minute after injection (P<0·05). Oestradiol levels in the ovarian vein blood did not change after epinephrine i.c.v. injection in rats on D2.To avoid any humoral influence, SONt and SONintact rats on D2 were injected i.c.v. with 5 µg epinephrine or with vehicle, and 5 min later the ovaries were incubated in vitro with or without LH. Under these conditions, it was demonstrated that the previous injection of epinephrine in SON-intact rats resulted in a diminished release of progesterone from ovaries incubated with or without LH.These results suggest that a central adrenergic stimulus increases progesterone release from the ovary on D1 and decreases it on D2. Also, this neural input would arrive at the ovary through the SON, and would condition the ovarian response to LH on D2. Ovarian progesterone changes could be attributed to signals coming from ganglionar neurons, which are affected by the central adrenergic stimulation.