Dopamine, infused at a rate of 4 mug/kg/min for 3-4 h unaccompanied by any significant changes in cardiovascular dynamics, induced a prompt and sustained suppression of circulating prolactin (PRL) levels in normal men and women as well as in patients with hyperprolactinemia. At the discontinuation of the infusion, there was a marked rebound in PRL levels in normal subjects and a rapid return to basal levels in hyperprolactinemic patients. Dopamine infusion also induced a significant fall in LH levels in the normal subjects with a marked rebound in LH levels following the infusion. No significant changes in GH, TSH, and FSH levels were observed. These data indicate that in man a dopaminergic mechanism ixists in the regulation of PRL secretion and that dopamine also exerts an inhibitory effect of LH release.

Total and free cortisol levels are significantly elevated in pregnancy, but the reasons for this are not clear. The relationships between the diurnal variation in saliva (free) cortisol and baseline levels of total cortisol, corticosterone-binding globulin (CBG), progesterone, and estrogens were studied in several groups of women (normal nonpregnant, taking a combined oral contraceptive pill, after superovulation therapy, during early and late pregnancy, and postpartum). Saliva cortisol levels were significantly elevated in late pregnancy throughout the day, with preservation of diurnal variation. Total cortisol and CBG levels were also significantly raised in pregnancy, but total cortisol levels were normal in women taking a combined oral contraceptive pill in spite of significantly elevated CBG. There was no relationship between saliva cortisol and progesterone levels, and it is unlikely that the increase in cortisol is due to displacement of cortisol from CBG by progesterone. Cortisol levels fell slowly postpartum over several days, making it improbable that the increase in cortisol is solely due to elevated CRH levels. It appears that increased free and total cortisol levels in pregnancy are related to resettingof the sensitivity of the hypothalamic-pituitary-adrenal axis and not merely to raised CBG, progesterone, or CRH levels.

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