The relevance of testosterone, oestradiol and certain peptides (oxytocin (OT), β-endorphin and prolactin (PRL)) to sexual arousal in humans is reviewed. In addition to behavioural studies, evidence of distribution of gonadal steroid receptors in the brain and the limited evidence from brain imaging are also considered. Testosterone plays a key role in the adult male, with clear, consistent evidence from studies of hypogonadal and eugonadal men. The roles of testosterone in the development of sexual arousability, and in the aging male, are less clear. The relevance of aromatization and of non-sexual effects of testosterone which might indirectly influence sexual arousal are not well understood. Testosterone in the female presents a more complex, less consistent picture. One possible explanation is a much greater variability across women in responsiveness to testosterone. A ‘desensitization hypothesis’ to account for the striking gender differences is offered. There is limited evidence of a direct effect of oestradiol on sexual arousability in women. The extent to which testosterone in women acts by conversion to oestradiol or by increase of free oestradiol is not yet clear. The role of peptides in sexual arousal remains uncertain, partly because of the multiple roles and sites of action of most peptides. OT and β-endorphin appear to have both excitatory and inhibitory effects. PRL has been proposed as an inhibitory factor via direct inhibition of dopaminergic activity, but the evidence for this is inconclusive. Whereas the traditional concept of ‘hormone’ continues to apply to the role of testosterone and oestradiol in sexual arousal, peptides present a more complex role.
M. W. BRINSMEAD, B. J. BANCROFT, G. D. THORBURN and M. J. WATERS
Hyperglycaemia was produced in chronically catheterized fetal lambs and pregnant ewes by the infusion of glucose into the fetus. Plasma concentrations of placental lactogen did not change significantly in either fetal or maternal circulations. Fetal and maternal hypoglycaemia was induced by administration of insulin to the fetus and ewe separately. Plasma concentrations of placental lactogen in the fetus did not change significantly but maternal plasma concentrations fell slightly after hypoglycaemia in either fetus or ewe. Plasma concentrations of placental lactogen rose in both the ewe and fetus during prolonged fasting of the ewe. These results neither confirm nor refute a role for placental lactogen in intermediary metabolism of the pregnant ewe and fetus but glucose concentration alone is unlikely to be a significant factor in the control of secretion of this hormone.
M. A. F. MURRAY, J. H. J. BANCROFT, D. C. ANDERSON, T. G. TENNENT and P. J. CARR
The endocrine effects of drugs on two groups of 12 male sexual offenders in a special hospital were studied. In the first study benperidol, chlorpromazine and placebo were compared and in the second ethynyl oestradiol and cyproterone acetate were compared with no treatment.
In the first study there was no difference between the three drugs in their effects on plasma testosterone or luteinizing hormone (LH). In the second study cyproterone acetate produced a reduction in plasma testosterone, LH and follicle-stimulating hormone (FSH). Ethynyl oestradiol produced a rise in plasma testosterone and LH, and no change in FSH. Neither drug changed total plasma oestrogen levels. The unexpected effects of ethynyl oestradiol were attributed to an increase in sex hormone-binding globulin (SHBG) leading to a rise in bound, inactive testosterone. Direct measurement showed a two- to threefold increase in SHBG with ethynyl oestradiol treatment and no change in SHBG with cyproterone acetate treatment. In spite of these contrasting endocrine effects, ethynyl oestradiol, cyproterone acetate and benperidol produced similar behavioural changes.