The effects of psychosomatic stress at the end of pregnancy on maternal and fetal plasma cortisol levels and liver glycogen in guinea-pigs

Dauprat, P; Monin, Gabriel; Dalle, M; Delost, P

doi:10.1051/rnd:19840105

Cited by 17 publications

(12 citation statements)

References 21 publications

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“…In rats, maternal and fetal plasma corticosterone are significantly elevated after maternal stress [79,105]. In the guinea pig, cortisol concentrations in the maternal plasma are 10-fold those in the fetus, and as for the rat, maternal stress results in significant increases in plasma glucocorticoid concentrations in both mother and fetus [81,106]. An important study has shown that greater glucocorticoid transfer occurs across the placenta of female compared to male fetuses [107].…”

Section: Glucocorticoids: the Endocrine Programming Factormentioning

confidence: 98%

RETRACTED: Maternal adversity, glucocorticoids and programming of neuroendocrine function and behaviour

Owen

Andrews

Matthews

2005

Neuroscience & Biobehavioral Reviews

196

148

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Section: Glucocorticoids: the Endocrine Programming Factormentioning

confidence: 98%

RETRACTED: Maternal adversity, glucocorticoids and programming of neuroendocrine function and behaviour

Owen

Andrews

Matthews

2005

Neuroscience & Biobehavioral Reviews

196

148

View full text Add to dashboard Cite

“…Animal studies suggest that glucocorticoids can be important ‘fetal programming’ factors in prenatal stress protocols. In rodent models prenatal stress has been shown to result in up‐regulation of glucocorticoid concentrations in both mother and fetus (Dauprat et al 1984; Cadet et al 1986) and excessive exposure of the fetus to maternal steroids may constitute at least part of the programming stimulus. (Dodic et al 1999; Seckl, 2001).…”

Section: Discussionmentioning

confidence: 99%

Prenatal stress alters cardiovascular responses in adult rats

Igosheva

Klimova

Anishchenko

et al. 2004

The Journal of Physiology

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Environmental factors in early life are clearly established risk factors for cardiovascular disease in later life. Most studies have focused on nutritional programming and analysed basal cardiovascular parameters rather than responses. In the present study we have investigated whether prenatal stress has long-term effects on cardiovascular responses in adult offspring. Female pregnant Sprague-Dawley rats were subjected to stress three times daily from day 15 to day 21 of gestation. Litters from stressed and control females were cross-fostered at birth to control for mothering effects. When the offspring were 6 months old, blood pressure was measured in the conscious rats through implanted catheters at rest, during restraint stress and during recovery. Basal haemodynamic parameters were similar in the different groups but the pattern of cardiovascular responses during stress and recovery differed markedly between prenatally stressed (PS) and control animals. PS rats had higher and longer-lasting systolic arterial pressure elevations to restraint stress than control animals. They also showed elevated systolic and diastolic blood pressure values during the recovery phase. PS rats demonstrated a greater increase in blood pressure variability compared with control animals during exposure to restraint stress, and showed more prolonged heart rate responses to acute stress and delayed recovery than controls. There was no effect of prenatal stress on baroreflex regulation of heart rate. PS females showed a greater increase in systolic arterial pressure and blood pressure variability and delayed heart rate recovery following return to the home cage then did PS males. These findings demonstrate for the first time that prenatal stress can induce long-term, sex-related changes in the sensitivity of the cardiovascular system to subsequent stress.

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“…In rats, maternal and fetal plasma corticosterone are significantly elevated after maternal stress (Takahashi et al, 1998;Koehl et al, 1999). In the guinea pig, cortisol concentrations in the maternal plasma are 10-fold those in the fetus, and as for the rat, maternal stress results in up-regulation of endogenous glucocorticoid concentrations in both mother and fetus (Dauprat et al, 1984;Cadet et al, 1986). Interestingly, it has been shown that greater endogenous glucocorticoid transfer occurs across the placenta of female compared to male fetuses (Montano and Wang, 1993).…”

Section: The 'Glucocorticoid Hypothesis'mentioning

confidence: 94%

Programming of the Hypothalamo–Pituitary–Adrenal Axis: Serotonergic Involvement

Andrews

Matthews

2004

Stress

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The ability of the early environment to programme the developing hypothalamo-pituitary-adrenal (HPA) axis has been reported in several animal species. There is considerable evidence that a similar process can occur in the human, and that long-term alterations in HPA function are associated with altered susceptibility to disease in later life. The phenotype of HPA function following early manipulation depends on the timing and intensity of the manipulation as well as the gender of the fetus/neonate. There is considerable interplay between the developing HPA and the reproductive axes and emerging evidence indicates that this interaction is modified by early environmental manipulation. Studies are rapidly unravelling the mechanisms that underlie developmental programming of the HPA axis. In this context, the serotonergic system has been identified as a primary system involved in this process. Understanding the mechanisms involved in neuroendocrine programming will facilitate the development of interventions aimed at reversing or ameliorating the impact of an adverse intrauterine environment.

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The effects of psychosomatic stress at the end of pregnancy on maternal and fetal plasma cortisol levels and liver glycogen in guinea-pigs

Cited by 17 publications

References 21 publications

RETRACTED: Maternal adversity, glucocorticoids and programming of neuroendocrine function and behaviour

RETRACTED: Maternal adversity, glucocorticoids and programming of neuroendocrine function and behaviour

Prenatal stress alters cardiovascular responses in adult rats

Programming of the Hypothalamo–Pituitary–Adrenal Axis: Serotonergic Involvement

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