Effect of estradiol implant on noradrenergic function and mood in menopausal subjects.

The effect of the alpha 2-adrenoceptor agonist, clonidine, on plasma growth hormone (GH), plasma 3-methoxy-4-hydroxyphenylethylenegylcol (MHPG), blood pressure and sedation were studied in 16 menopausal subjects before and 6 wk after a 100-mg implant of estradiol. The specific binding of tritiated yohimbine to intact platelets also was studied. Estradiol implants increased basal GH output and reduced baseline MHPG and sedation scores. However, none of the subsequent responses to clonidine were altered. Platelet yohimbine binding also was unchanged following the implant. Both observer- and self-rating scales showed a marked reduction in anxiety and depression scores. The results suggest that estradiol may alter some indices of noradrenergic function, but that the mechanism does not involve alterations in alpha 2-adrenoceptor sensitivity.

Effect of oestradiol treatment on 5-HT and dopamine-mediated neuroendocrine responses.

We assessed the effect of oestradiol treatment in women on the endocrine responses to the 5-hydroxytryptamine (5-HT) precursor, L-tryptophan (LTP) (5 g i.v.) and the dopamine agonist, apomorphine (0.005 mg/kg s.c.). Following oestradiol implant (100 mg s.c.) the prolactin (PRL) response to LTP was significantly enhanced but there was no change in the growth hormone (GH) response to apomorphine. There was, however, a significant correlation between post-implant oestradiol concentrations and post-implant apomorphine-induced GH release. The results indicate that oestrogen treatment may facilitate 5-HT-mediated PRL release and could also influence the regulation of dopamine-mediated GH responses. However, further studies are needed to exclude direct effects of oestradiol on the pituitary release of PRL and GH.

Binding of tritiated yohimbine to platelets in women with maternity blues.

Platelet alpha 2-adrenoceptor binding was measured in 108 women in the 36th week of pregnancy, at ten and twenty days and at three and six months post-partum. An age matched non-pregnant control group of women (N = 25) was also studied. The number (Bmax) of alpha 2-adrenoceptors was elevated antepartum but fell to control values on the tenth post-partum day. At three and six months post-partum, however, alpha 2-adrenoceptor Bmax was again increased. Women who developed maternity blues (N = 59) had significantly more platelet alpha 2-adrenoceptors than those who did not (N = 49) at both ten and twenty days post-partum. In addition their alpha 2-adrenoceptor Bmax was greater than controls at all time points measured except the tenth post-partum day. In contrast, the alpha 2-adrenoceptor Bmax of women without the blues did not differ from controls at any stage. It is suggested that women who develop maternity blues may have a relatively enduring abnormality in alpha 2-adrenoceptor sensitivity which is associated with psychological symptoms when concentrations of circulating sex-steroids suddenly change.