The physiological roles of placental corticotropin releasing hormone in pregnancy and childbirth

Abstract

In response to stress, the hypothalamus releases cortiticotropin releasing hormone (CRH) that travels to the anterior pituitary, where it stimulates the release of adrenocorticotropic hormone (ACTH). ACTH travels to the adrenal cortex, where it stimulates the release of cortisol and other steroids that liberate energy stores to cope with the stress. During pregnancy, the placenta synthesises CRH and releases it into the bloodstream at increasing levels to reach concentrations 1,000 to 10, 000 times of that found in the non-pregnant individual. Urocortins, which are CRH analogues are also secreted by the placenta. Desensitisation of the maternal pituitary to CRH and resetting after birth may be a factor in post-partum depression. Recently, CRH has been found to modulate glucose transporter (GLUT) proteins in placental tissue, and therefore there may be a link between CRH levels and foetal growth. Evidence suggests CRH is involved in the timing of birth by modulating signalling systems that control the contractile properties of the myometrium. In the placenta, cortisol stimulates CRH synthesis via activation of nuclear factor kappa B (NF-κB), a component in a cellular messenger system that may also be triggered by stressors such as hypoxia and infection, indicating that intrauterine stress could bring forward childbirth and cause low birth weight infants. Such infants could suffer health issues into their adult life as a result of foetal programming. Future treatment of these problems with CRH antagonists is an exciting possibility.

Second-trimester amniotic fluid corticotropin-releasing hormone and urocortin in relation to maternal stress and fetal growth in human pregnancy

“…Whether acute maternal stress affects fetoplacental CRH or UCN levels has hardly been investigated so far (Thomson, 2013), and our study aimed to contribute to the literature in this field.…”

“…One underinvestigated question in this connection is whether the acute maternal stress response affects fetoplacental CRH and/or UCN levels (Thomson, 2013).…”

Aflatoxin B1 augments the synthesis of corticotropin releasing hormone in JEG-3 placental cells

“…According to these reports, the effective dosage that could initiate changes in CRH synthesis in the present study fell in the physiological range. As placental CRH modulates labor induction, glucose transport to the fetus, an untimely surge of CRH may result in preterm birth and low birth weight infants [31]. Results of the current study implicate a role of aflatoxin exposure in preterm delivery and low birth weight infant, especially in the humid tropics.…”

DIAGNOSIS OF ENDOCRINE DISEASE: Differentiation of pathologic/neoplastic hypercortisolism (Cushing’s syndrome) from physiologic/non-neoplastic hypercortisolism (formerly known as pseudo-Cushing’s syndrome)

“…The increase in plasma ACTH has been attributed to the secretion of CRH from the placenta, the increase in progesterone acting as a glucocorticoid antagonist, a decrease in glucocorticoid negative feedback sensitivity and the production of ACTH from the placenta (63). CRH-binding protein also increases during pregnancy, which may prevent the stimulatory effects of placental CRH on the maternal pituitary gland (67,68,69). The actual diagnosis of Cushing's syndrome is uncommon in pregnancy as hypercortisolism usually attenuates hypothalamic-pituitary-gonadal function.…”