Our working hypothesis was that the negative feedback effect of progesterone on LH secretion in ovariectomised cows is greatly enhanced by oestradiol when both hormones are administered intravaginally. Each of eight ovariectomised cows had a progesterone releasing device ('CIDR-1'; Eazi-breed CIDR-B. InterAg, Hamilton, New Zealand) inserted into the vagina for 3 days, followed by an injection of 1 mg oestradiol benzoate (ODB) in peanut oil 24 h after device removal. The timing of this injection was designated as Day 0. The CIDR-1 was reinserted concurrently with an injection of 0.4 mg ODB on Day 5. An additional device ('CIDR-2') was inserted 4 days later (Day 9). In four of the cows, an ODB capsule (CIDIROL), Douglas Pharmaceuticals. Auckland, New Zealand) was placed into a groove on the surface of CIDR-2 preceding insertion. CIDR-2 was withdrawn after 5 days (Day 14) and CIDR-1 was withdrawn 2 days later (Day 16). The treatment regimen was repeated in a cross-over design where each cow received CIDR-2 with or without an ODB capsule. Blood samples were collected at intervals of 15 min for a period of 16 h beginning 8 h before insertion of CIDR-2 to determine changes in LH secretion pattern, and then at intervals of 8 h until 48 h after removal of CIDR-1 to determine mean LH and steroid concentrations. Concentrations of progesterone in plasma reflected the effects of inserting and removing each CIDR device. The insertion of CIDR-2 elevated progesterone from 2.0 +/- 0.1 ng ml-1 to 4.9 +/- 0.1 ng ml-1 within 30 min (P < 0.01) and maintained levels > 3 ng ml-1. Withdrawal of CIDR-2 produced a new baseline level of 1.8 +/- 0.1 ng ml-1 within 4 h (P < 0.01). Concentrations of oestradiol-17 beta in plasma increased from a baseline of < 1 pg ml-1 to-a-maximum of 12.6 +/- 2.2 pg ml-1 at 22 h after insertion of an ODB capsule. Initial pulse frequency of LH (1.2 +/- 0.05 pulses h-1) and mean concentration of LH (1.6 +/- 0.1 ng ml-1) declined (P < 0.05) to 0.2 +/- 0.1 pulses h-1 and 0.5 +/- 0.1 ng ml-1 during the period from 2 to 8 h following insertion of CIDR-2. Mean concentrations recovered to pre-treatment levels (> 1 ng ml-1) within 48 h if CIDR-2 was inserted without an ODB capsule. In contrast, LH levels remained less than 0.7 ng ml-1 for 5 days following this form of ODB treatment. A subsequent increase in mean LH of 1.4 +/- 0.2 ng ml-1 (P < 0.05) was inversely synchronised with the precipitous decline in progesterone of 1.2 +/- 0.1 ng ml-1, following removal of CIDR-2. The inclusion of an ODB capsule with insertion of CIDR-2 reduced concentrations of FSH from 166 +/- 17 ng ml-1 to a new baseline of 105 +/- 16 ng ml-1 within 24 h (P < 0.05). In conclusion, an acute increase in progesterone induced a transient suppression of LH lasting less than 48 h. This suppression was prolonged to 5 days by the concurrent insertion of a capsule containing 10 mg ODB. The subsequent recovery of LH was coincident with the decline in progesterone following removal of CIDR-2.