Postnatal disappearance of the pregnancy-associated reduced sensitivity of plasma cortisol to feedback inhibition

Owens, P. C.; Smith, Roger; Brinsmead, Maxwell; Hall, Chris; Rowley, Maralyn; Hurt, Dianne; Lovelock, Margaret; Chan, Eng‐Cheng; Cubis, Jeff; Lewin, Terry J.

doi:10.1016/0024-3205(87)90603-5

Cited by 621 publications

(31 citation statements)

References 72 publications

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“…In humans, previous work suggests a reduced responsivity of the hypothalamus-pituitary-adrenal (HPA) axis, a major neuroendocrine stress pathway, to acute stimulation as pregnancy advances (Kammerer, Adams, Castelberg Bv, & Glover, 2002;Owens et al, 1987;Schulte, Weisner, & Allolio, 1990). A similar pattern has been reported for cardiovascular (Barron, Mujais, Zinaman, Bravo, & Lindheimer, 1986;Matthews & Rodin, 1992;Nisell, Hjemdahl, Linde, & Lunell, 1985b), sympathoadrenal (Barron et al;Nisell, Hjemdahl, Linde, & Lunell, 1985a;Whittaker, Gerrard, & Lind, 1985), and affective responses (Glynn, Wadhwa, Dunkel-Schetter, Chicz-Demet, & Sandman, 2001).…”

Section: Introductionmentioning

confidence: 62%

“…For example, ACTH but not plasma cortisol responses to stimulation with 1 mg/kg oCRH were clearly blunted at 3 and 6 weeks after the end of pregnancy and still slightly reduced at 12 weeks postpartum (Magiakou et al, 1996). In contrast, parity was reported to have an influence on dexamethasone-suppressed plasma cortisol levels until about the third postnatal week, while this insensitivity to feedback inhibition was absent by the fifth week postpartum (Owens et al, 1987). Finally, a lack of significant salivary cortisol responses to a cold pressor test was observed at 8 weeks postpartum (Kammerer et al, 2002).…”

Section: Introductionmentioning

confidence: 81%

“…While previous studies clearly demonstrate reduced feedback sensitivity and attenuated responsivity of the HPA axis during pregnancy (Kammerer et al, 2002;Owens et al, 1987;Schulte et al, 1990), the few studies that were conducted after pregnancy in the postpartum period (Kammerer et al, 2002;Magiakou et al, 1996;Owens et al, 1987) revealed inconclusive results and have relied on small sample sizes. Only one previous study assessed HPA axis activity later in life and suggests significantly lower baseline plasma cortisol levels in postmenopausal women with five or more children as compared to women with two or less children.…”

Section: Parity and Hpa Axis Functionmentioning

confidence: 91%

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Parity does not alter baseline or stimulated activity of the hypothalamus-pituitary-adrenal axis in women

et al. 2006

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Pregnancy is associated with considerable physiological adaptations, some of which long outlast the state of pregnancy. Although it is well documented that pregnancy produces alterations of the hypothalamus-pituitary-adrenal axis, the longer-term effects of pregnancy on this system have not been systematically examined in humans. Subjects in the present study were 159 nulliparous and 265 parous women. Data analysis revealed no impact of parity on baseline activity (salivary cortisol: response to awakening, F

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Section: Introductionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 81%

Section: Parity and Hpa Axis Functionmentioning

confidence: 91%

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Parity does not alter baseline or stimulated activity of the hypothalamus-pituitary-adrenal axis in women

et al. 2006

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“…An enhanced glucocorticoid feedback especially at hippocampal, but also hypothalamic, brain areas would negatively control CRHÏvasopressin neurons and, thus, attenuate ACTH secretion. With respect to glucocorticoid feedback control during pregnancy, various species-dependent results have been published with unchanged (Keller-Wood, 1996) or reduced feedback sensitivity (Owens et al 1987). Changes in glucocorticoid receptor binding capacity within the hippocampus as observed in lactation (Meaney, Viau, Aitken & Bhatnagar, 1989) are being studied in our laboratories also during pregnancy (Johnstone et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Attenuated neuroendocrine responses to emotional and physical stressors in pregnant rats involve adenohypophysial changes

Neumann

Johnstone

Hatzinger

et al. 1998

The Journal of Physiology

341

244

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1. The responsiveness of the rat hypothalamo-pituitary-adrenal (HPA) axis and hypothalamo-neurohypophysial system (HNS) to emotional (elevated plus-maze) and physical (forced swimming) stressors and to administration of synthetic corticotrophinreleasing hormone (CRH) was investigated during pregnancy and lactation. In addition to pregnancy-related adaptations at the adenohypophysial level, behavioural responses accompanying the neuroendocrine changes were studied. 2. Whereas basal (a.m.) plasma corticosterone, but not corticotrophin (adrenocorticotrophic hormone; ACTH), levels were increased on the last day (i.e. on day 22) of pregnancy, the stress-induced rise in both plasma hormone concentrations was increasingly attenuated with the progression of pregnancy beginning on day 15 and reaching a minimum on day 21 compared with virgin control rats. A similar attenuation of responses to both emotional and physical stressors was found in lactating rats. 3. Although the basal plasma oxytocin concentration was elevated in late pregnancy, the stressinduced rise in oxytocin secretion was slightly lower in day 21 pregnant rats. In contrast to vasopressin, oxytocin secretion was increased by forced swimming in virgin and early pregnant rats indicating a differential stress response of these neurohypophysial hormones. 4. The blunted HPA response to stressful stimuli is partly due to alterations at the level of corticotrophs in the adenohypophysis, as ACTH secretion in response to CRH in vivo (40 ng kg¢, i.v.) was reduced with the progression of pregnancy and during lactation. In vitro measurement of cAMP levels in pituitary segments demonstrated reduced basal levels of cAMP and a lower increase after CRH stimulation (10 nÒ, 10 min) in day 21 pregnant compared with virgin rats, further indicating reduced corticotroph responsiveness to CRH in pregnancy. 5. The reduced pituitary response to CRH in late pregnancy is likely to be a consequence of a reduction in CRH receptor binding as revealed by receptor autoradiography.[ÁÂÇI]CRH binding in the anterior pituitary was significantly reduced in day 11, 17 and 22 pregnant rats compared with virgin controls. 6. Anxiety-related behaviour of the animals as revealed by the time on and entries into the open arms of the elevated plus-maze was different between virgin and pregnant rats with decreased number of entries indicating increased anxiety with the progression of pregnancy (except on pregnancy day 18). The emotional behaviour, however, was not correlated with the neuroendocrine responses. 7. The results indicate that the reduced response of the HPA axis to stressors described previously during lactation is already manifested around day 15 of pregnancy in the rat and involves physiological adaptations at the adenohypophysial level. However, alterations in stressor perception at higher brain levels with the progression of pregnancy may also be involved.

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“…Following delivery of the placenta, there is a sharp drop in placental CRH levels. The HPA axis is relatively hyporesponsive with lack of cortisol suppression to dexamethasone for up to 3 weeks postpartum [60] and dynamic tests showing recovery of CRH secretion by 12 weeks postpartum [61] . ACTH levels also fall transiently immediately after delivery, rising again 3-4 days postpartum [62] .…”

Section: The Maternal Hpa Axismentioning

confidence: 99%

Changes in the Maternal Hypothalamic-Pituitary-Adrenal Axis in Pregnancy and Postpartum: Influences on Maternal and Fetal Outcomes

Duthie¹,

Reynolds²

2013

Neuroendocrinology

274

221

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Overexposure of the developing fetus to glucocorticoids is hypothesised to be one of the key mechanisms linking early life development with later life disease. The maternal hypothalamic-pituitary-adrenal (HPA) axis undergoes dramatic changes during pregnancy and postpartum. Although cortisol levels rise threefold by the third trimester, the fetus is partially protected from high cortisol by activity of the enzyme 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2). Maternal HPA axis activity and activity of HSD11B2 may be modified by maternal stress and disease allowing greater transfer of glucocorticoids from mother to fetus. Here we review emerging data from human studies linking dysregulation of the maternal HPA axis to outcomes in both the mother and her offspring. For the offspring, greater glucocorticoid exposure is associated with lower birth weight and shorter gestation at delivery. In addition, evidence supports longer term consequences for the offspring including re-setting of the HPA axis and susceptibility to neurodevelopmental problems and cardiometabolic disease. For the mother, the changes in the HPA axis, particularly in the postpartum period, may increase vulnerability to mood disturbances. Further understanding of the changes in the HPA axis during pregnancy and the impact of these changes may ultimately allow early identification of those most at risk of future disease.

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Postnatal disappearance of the pregnancy-associated reduced sensitivity of plasma cortisol to feedback inhibition

Cited by 621 publications

References 72 publications

Parity does not alter baseline or stimulated activity of the hypothalamus-pituitary-adrenal axis in women

Parity does not alter baseline or stimulated activity of the hypothalamus-pituitary-adrenal axis in women

Attenuated neuroendocrine responses to emotional and physical stressors in pregnant rats involve adenohypophysial changes

Changes in the Maternal Hypothalamic-Pituitary-Adrenal Axis in Pregnancy and Postpartum: Influences on Maternal and Fetal Outcomes

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