Sixteen individually caged adult female vervet monkeys (Cercopithecus aethiops), whose reproductive parameters had been studied for 5 years, were hysterectomized/ovariectomized during three reproductive states; i.e. the late follicular (15·4 ± 4·7 (s.d.) days) and luteal (27·8 ± 4·7 days) phases of the normal cycle (20–50 days), and during prolonged intermenstrual intervals (PII; 99·0 ± 2·5 days since the previous menses). These latter animals showed characteristics of both follicular and luteal phases; i.e. their ovaries contained both corpora lutea and large antral follicles and systemic oestradiol and progesterone concentrations were raised. Analysis of cytoplasmic oestrogen and progestin receptors (CER and CPR) revealed that endometrium during PII had CER levels of 0·58 ± 0·07 pmol/mg protein, similar to those of the follicular phase (0·60 ± 0·12); CPR levels (1·20 ± 0·87) were not different from those of the luteal phase (1·05 ± 0·45). The ratio of CPR to CER during the luteal phase was about tenfold higher than that of the follicular phase. Levels during PII were intermediate between the two phases. Under receptoractivating conditions, the DNA-binding components of the PII cytoplasmic fraction underwent over 40% loss while those present during both phases of the normal cycle doubled. The hormone-binding sites at all times remained intact indicating that the DNA and hormone-binding sites are distinct on both CER and CPR.
Less than 50% interaction of CER/CPR with DNA-cellulose was obtained, indicating the presence of only limited quantities of cytoplasmic activating factors which may be a prerequisite for receptor binding to the genome. During PII, factors which deactivate DNA-binding sites may also have been induced. Extensive accumulation of nuclear oestrogen receptor was evident in PII endometrium with 80% being salt-resistant. This level is higher than that in the follicular and luteal phases (37 and 52% respectively). These data, suggesting a possible aberration of receptor activation in vitro and receptor processing in vivo, may be indicative of endometrial dysfunction during PII. This could lead to a delay in menstruation.