Hypothalamo-pituitary-adrenal axis responses to stress are attenuated perinatally, and may contribute towards conservation of energy stores and/or prevention of overexposure to glucocorticoid and its adverse effects in the developing fetus/neonate. Previous work has shown that reduced central drive to the hypothalamo-pituitary-adrenal axis is responsible, since parvocellular paraventricular nucleus neurone responses are reduced. One of the main input pathways to the paraventricular nucleus that is activated by the majority of stressors is the brainstem noradrenergic system. This review outlines key noradrenergic mechanisms that mediate hypothalamo-pituitary-adrenal axis responses to acute stress, and addresses aspects of their adaptation in pregnancy and lactation that can explain the stress hyporesponsiveness at that time. In summary, reduced noradrenaline release and adrenergic receptor expression in the paraventricular nucleus may lead to reduced sensitivity of the hypothalamo-pituitary-adrenal axis to adrenergic antagonists and agonists and its responses to stress. While there are subtle differences in these changes between pregnancy and lactation, it would appear that reduced effectiveness of the noradrenergic input can at least partly account for the reduced hypothalamo-pituitary-adrenal axis responses both pre- and post-natally.