Increased adrenocortical responsiveness to exogenous ACTH in oral contraceptive users

Abstract

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.

Cerebrospinal Fluid Corticotropin-Releasing Factor (CRF) and Vasopressin Concentrations Predict Pituitary Response in the CRF Stimulation Test: A Multiple Regression Analysis

“…Since oral contraceptives have been associated with altered HPA axis measures including lower concentrations of ACTH (Carr et al, 1979;Nickelsen et al, 1989), elevated concentrations of cortisol (Carr et al, 1979;Nickelsen et al, 1989;Meulenberg and Hofman, 1990) and cortisol binding globulin (Bulbrook et al, 1973;Carr et al, 1979;Carol et al, 1980;Fujimoto et al, 1986;Kirschbaum et al, 1999), and diminished salivary cortisol responses to various stressors (Kirschbaum et al, 1995(Kirschbaum et al, , 1996(Kirschbaum et al, , 1996, the holdout sample approach (Kleinbaum et al, 1998) was used to assess the impact of oral contraceptive use upon the reliability of the model. To implement this approach, a second regression analysis was performed using the same dependent variable and predictor variables against the holdout sample of participants who were not taking oral contraceptives.…”

Hormonal contraception use alters stress responses and emotional memory

“…Women on oral contraceptives had similar salivary cortisol responses to TSST compared to women in the follicular phase of the menstrual cycle, but significantly blunted responses compared to men and women in the luteal phase of the menstrual cycle. These findings suggest that oral contraceptive use can alter HPA activity in response to a psychosocial stressor, and these effects are likely due to the corticosteroid-binding globulin (CBG) enhancing effect of ethinyl estradiol (Fujimoto et al, 1986; Kirschbaum et al, 1999; Kumsta et al, 2007). …”

Postlearning stress differentially affects memory for emotional gist and detail in naturally cycling women and women on hormonal contraceptives.

“…Sex hormone influences on HPA and sympathetic nervous system (SNS) activity are observable when menstrual cycle phase and oral contraceptive use are accounted for in women; both circulating levels of endogenous and exogenous sex hormones appear to play a key role in modulating HPA and SNS function (Kudielka & Kirschbaum, 2005; Fujimoto et al, 1986; Kirschbaum et al, 1999; Kumsta et al, 2007). …”

“…Evidence for the relationship between sex and stress hormone activity in humans comes from studies demonstrating that menstrual cycle phase and hormonal contraceptive use have profound effects on stress hormone reactivity (Bentz et al, 2013; Kirschbaum, Kudielka, Gaab, Schommer, & Hellhammer 1999; Nielsen, Segal, et al, 2013; Otterstetter et al, 1999). Sex hormone influences on HPA and sympathetic nervous system (SNS) activity are observable when menstrual cycle phase and oral contraceptive use are accounted for in women; both circulating levels of endogenous and exogenous sex hormones appear to play a key role in modulating HPA and SNS function (Fujimoto, Willanueva, Hopper, Moscinski, & Rebar, 1986; Kirschbaum et al, 1999; Kudielka & Kirschbaum, 2005; Kumsta, Entringer, Hellhammer, & Wüst, 2007).…”