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Indeed, the administration of betamethasone to women in premature labor at 2832 weeks of pregnancy has not been observed to produce a consistent effect on maternal CRH levels, even though plasma ACTH and cortisol are suppressed.181, 204, 205 In experimental models of acute fetal hypoxemia induced in sheep by compression of the uterine artery or by infusion of adrenaline into the fetal circulation, CRH concentrations rise in the fetal and maternal plasma.195, 206 The increase in fetal CRH is probably from a reduction in uteroplacental blood flow, which causes the release of catecholamines that trigger CRH secretion in both the fetus and the placenta.207 A role for catecholamines is suggested by the fact that noradrenaline and adrenaline stimulate CRH release by human placental cells.200 The stimulatory actions of these catecholamines are mimicked by 1- and 2-adrenergic receptor agonists and are blocked by 1- and 2-receptor antagonists
Existing human data do not support obvious fertility advantages
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Acknowledgments The corresponding author, AS, is thankful to authors for their collaborative efforts in writing this paper
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