Sensitivity to stress-induced reproductive dysfunction is associated with a selective but not a generalized increase in activity of the adrenal axis.
Stress-induced reproductive dysfunction is a relatively common cause of infertility in women. In response to everyday life stress, some individuals readily develop reproductive dysfunction (i.e., they are stress sensitive), whereas others are more stress resilient. Female cynomolgus monkeys, when exposed to mild combined psychosocial and metabolic stress (change in social environment + 20% reduced calorie diet), can be categorized as stress sensitive (SS; they rapidly become anovulatory in response to stress), medium stress resilient (MSR; they slowly become anovulatory in response to prolonged stress), or highly stress resilient (HSR; they maintain normal menstrual cycles in response to stress). In this study, we examined whether increased sensitivity to stress-induced reproductive dysfunction is associated with elevated adrenal axis activity by measuring 1) the diurnal release of ACTH and cortisol, 2) ACTH and cortisol in response to an acute psychological stress, 3) the percent suppression of cortisol in response to dexamethasone negative feedback, 4) the diurnal release of ACTH and cortisol following exposure to mild psychosocial and metabolic stress, 5) the concentration of cortisol in hair, and 6) adrenal weight. SS monkeys (n = 5) did not differ from MSR (n = 5) or HSR (n = 7) monkeys in any measurement of baseline HPA axis activity or the integrated measurements of chronic HPA axis activity. However, MSR + SS monkeys (n = 10) did secrete more cortisol than HSR monkeys during the daytime hours (1000-1800) following exposure to a novel social environment and reduced diet. We conclude that increased activity of the HPA axis is unlikely to be the primary mechanism causing increased sensitivity to stress-induced reproductive dysfunction.
Department of Behavioral Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon, USA.
S M
SM
Herod
A M
AM
Dettmer
M A
MA
Novak
J S
JS
Meyer
J L
JL
Cameron
D000311:Adrenal Glands / Q000033:anatomy & histology / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000568:Amenorrhea / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D000818:Animals; D002940:Circadian Rhythm; D003907:Dexamethasone / Q000494:pharmacology; D004032:Diet / Q000009:adverse effects; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006197:Hair / Q000737:chemistry; D006234:Handling, Psychological; D006854:Hydrocortisone / Q000032:analysis / Q000097:blood; D007247:Infertility, Female / Q000503:physiopathology; D008252:Macaca fascicularis; D009929:Organ Size; D012931:Social Environment; D013315:Stress, Psychological / Q000097:blood / Q000503:physiopathology*
D005938:Glucocorticoids; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone