Control of neurohypophysial hormone secretion, blood osmolality and volume in pregnancy

In pregnancy, blood volume increases greatly and plasma osmolality is reduced, due to mild hyponatraemia despite sodium retention. In rats, both vasopressin and oxytocin neurones in the supraoptic nucleus are osmosensitive and have contrasting roles in these adaptations. Increased vasopressin secretion stimulates water retention by renal actions, while oxytocin is natriuretic, partly by stimulating cardiac atrial natriuretic peptide (ANP) secretion. In pregnancy, relaxin from the corpora lutea, acting via the lamina terminalis in the presence of pregnancy levels of oestrogen and progesterone, stimulates vasopressin secretion and drinking, resulting in hypervolaemia and hyponatraemia. Initial stimulation of oxytocin secretion by relaxin is lost in late pregnancy, and oxytocin neurone responses to modest osmotic stimulation are reduced. Consequently, with reduced ANP secretion and action, sodium is retained and hypervolaemia maintained. Oxytocin neurone responses to other inputs, from hypervolaemia, immune or satiety signals, are reduced in late pregnancy by up-regulated central endogenous opioid mechanisms. Neither inhibition by opioid nor nitric oxide explains reduced responses to osmotic stimulation. Increased activity of GABA input, by allopregnanolone action, might be involved. However, the lack of a shift in threshold for hyperosmotic stimulation of oxytocin secretion in pregnancy, despite the hyponatraemia caused by relaxin, seems a sufficient explanation.