The endocrine and ovarian responses to prolonged adrenal stimulation at the time of corpus luteum (CL) regression were studied in non-lactating non-pregnant Friesian cows. Cows were synchronized with two cloprostenol (PG) injections 11 days apart (second PG referred as time 0). Experiment 1 was carried out on five animals in two phases with a resting period in between. Between -48 and 84 h, animals received 12 injections of either saline (CTR) or adrenocorticotrophic hormone (ACTH) agonist (Synacthen; SYN) every 12 h. Cortisol (C), progesterone (P4), oestradiol (E2) and LH were analysed in the blood samples collected every 8-12 h between days -3 and 4. Pulsatile LH release was studied 4 h before and 4 h after naloxone administration beginning at 96 h. Experiment 2 was carried out on four cows in a cross-over experimental design (two phases, with a resting period in between). Treatments were performed by administering either saline (CTR) or Synacthen (SYN) every 12 h between -36 and 24 h. The concentrations of C, P4 and E2 were measured in blood plasma every 4-12 h from days -3 to 3, then every day from days 5 to 9. In both experiments, ovaries were examined by ultrasonography every 1-3 days. ACTH administration induced a significant increase (p < 0.001) of plasma C lasting for 7 days (experiment 1), and for 3-4 days (experiment 2). Plasma C returned to baseline levels within 6 days (expt 1) or 36 h (expt 2) after treatment interruption. During the SYN phase, LH pre-ovulatory surge was not detectable. During the CTR phase, naloxone administration induced a significant increase (p < 0.05) of average LH concentrations that was not evident during the SYN phase. The dominant follicle development was retarded and mean plasma E2 concentrations were significantly lower during the SYN phase (p < 0.01). Luteolysis was completed within 2 days. However, P4 decline between 0 and 4 h was slower (p < 0.01) during the SYN phase. Our results indicate that, under prolonged adrenal stimulation, follicular development is delayed and LH release is impaired, which are independent of CL function.