Midluteal Research Articles

Increased adrenocortical responsiveness to exogenous ACTH in oral contraceptive users.

To evaluate the effects of changing steroid milieu on adrenocortical function, basal levels and responses of cortisol, 17-hydroxyprogesterone (17PO), androstenedione (A), dehydroepiandrosterone (DHEA), and testosterone to exogenous synthetic ACTH were investigated in six normal women during the early follicular (EF) and midluteal (ML) phases of the menstrual cycle and in five women on an oral contraceptive (OC) agent (35 micrograms ethinyl estradiol and 1 mg ethynodiol diacetate, Demulen). Baseline serum steroid and cortisol binding globulin (CBG) levels were measured on days 3-7 and 21-23 of the menstrual cycle in the normal subjects and on days 3-7 of OC treatment cycles. ACTH stimulation (10 micrograms m-2 i.v. bolus) was performed following dexamethasone suppression (0.5 mg p.o. q 6 h X 4). Basal levels of cortisol and CBG as well as cortisol responses to ACTH were increased in OC users relative to normal women tested during both the EF and ML phases of the cycle. In addition, 17PO levels were increased during the ML phase both before and following dexamethasone suppression compared to levels present in the EF phase and in OC users, no doubt because of increased ovarian steroidogenesis.

Temporal Relationship of the Pulsatile Fluctuation of Luteinizing Hormone and Progesterone in Cattle: A Time Series Cross-Correlation Analysis

The temporal relationship between the pulsatile patterns of plasma luteinizing hormone (LH) and progesterone (P4) was studied in mid-luteal (ML) and early-pregnant (EP) dairy cows. Blood samples were collected (via external jugular vein cannulae) at 10-min intervals for 16 h in 5 ML cows (d 10 to 12 of the cycle) and for 10 h in 5 EP cows (d 52 to 56 of gestation). Concentrations of LH and P4 were determined by radioimmunoassays and a time series cross-correlation analysis was utilized to evaluate the temporal relationship between them. A pulsatile pattern was found for both hormones in both groups, and in all animals LH peaks were uniformly followed by P4 peaks. In 80% of the cows in both groups the highest cross-correlation occurred between samples LH(n) and P4 (n + 1) (n = sample number), suggesting that a lag time of about 10 min is necessary for luteal stimulation. Results from both groups demonstrate that P4 is released from the corpus luteum in a pulsatile manner and that its release is at least partially dependent upon the pulsatile pattern of plasma LH. Correlation coefficients between LH and P4 mean level, basal levels, peak frequencies and peak amplitudes obtained in both groups indicate that the conceptus alters the hypothalamic-pituitary-ovarian relationship found in the ML cows, suggesting the existence of another factor(s) acting along with LH to release P4 in EP cows.

The effects of estrogen and progestin on endogenous opioid activity in oophorectomized women.

Sex steroids may modulate the secretion of beta-endorphin (beta-EP). Naloxone (Nal), an opioid antagonist, has been used as a probe of central opioid activity. Nal-evoked responses of PRL and LH were evaluated in the midluteal (ML) and late follicular (LF) phases of ovulatory women (Pre) and compared to responses of oophorectomized women before and after the administration of conjugated estrogens (CE) and again after CE and progestin administration. In the ML and LF phases, serum LH increased significantly (P less than 0.05 and P less than 0.01, respectively) during Nal infusion for 4 h, while PRL did not change. In oophorectomized women, there were no significant changes in LH or PRL during Nal infusion. After 3 weeks of CE treatment (1.25 mg daily), LH increased during Nal infusion (P less than 0.05), as did PRL (P less than 0.01). After treatment with CE and medroxyprogesterone acetate (MPA), LH and PRL both increased (P less than 0.05 and P less than 0.01, respectively). The area under the LH curve during Nal infusion after CE and MPA treatment was greater than that after CE alone. Both of these responses were comparable to those of the LF and ML phases of Pre women. During Nal infusion, LH pulse frequency increased in the ML compared to the LF phase of the cycle and, in oophorectomized women, was greater after CE and CE with MPA treatment compared to pretreatment values (P less than 0.05). LH amplitudes during Nal infusion were highest in the ML phase and after CE and MPA treatment in oophorectomized women, and these LH amplitudes were similar. No correlation was found between peripheral plasma beta-EP and Nal-evoked LH responses. No differences were evident in plasma beta-EP levels between Pre and oophorectomized women. In conclusion, 1) endogenous opioid activity is low in oophorectomized women; 2) treatment with estrogen increases opioid activity, and the addition of a progestin increases this activity further; and 3) these data support the contention that sex steroids exert a profound influence on endogenous opioid activity.