| Abstract: | A chronic anovulatory polycystic ovarian (PCO) condition can be induced in rats with estradiol valerate (EV). We have previously shown that the early stages (8-10 wk after EV treatment) of the condition are characterized by low basal plasma luteinizing hormone (LH) and estradiol concentrations, as well as poor LH responsiveness to LH-releasing hormone (LHRH). These observations suggested that alterations in pituitary LH secretory activity may be involved in induction and maintenance of the PCO condition. In order to examine this possibility we have measured basal plasma LH and follicle-stimulating hormone (FSH) concentrations at various times (6, 15, 20 and 22 wk) after treatment with EV. AT 22 wk animals were subjected to a double LHRH pulse or equivalent treatment with saline. Basal plasma LH concentrations in EV-treated animals doubled between 6 and 22 wk. Despite this sharp increase, basal plasma LH concentrations at 22 wk were still significantly lower in EV-treated animals compared to proestrous controls. Basal FSH in EV-treated animals, remained in the proestrous range throughout the 22-wk period. Pituitary FSH and LH secretions in response to the LHRH challenge were significantly greater in EV-treated animals compared to proestrous controls. Plasma estradiol was significantly greater at 22 wk post-EV treatment than at 9 wk and this difference was reflected in the histology of the endometrium. These results indicate that a PCO condition is compatible with radical alterations in basal LH, and responsiveness to LHRH. Thus, aberrations in the ability to secrete LH do not appear to be causal in maintaining the condition. |
