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The psychoneuroendocrine responses to sexual arousal have not been clearly established in humans. However, we have demonstrated previously that masturbation-induced orgasm stimulates cardiovascular activity and induces increases in catecholamines and prolactin in blood of both males and females. We presently investigated the role of orgasm in producing these effects. Therefore, in this study parallel analysis of prolactin, adrenaline, noradrenaline, and cortisol concentrations, together with cardiovascular variables of systolic/diastolic blood pressure and heart rate were undertaken during film-induced sexual arousal in nine healthy adult men and nine healthy adult women. Blood was drawn continuously via an indwelling cannula and connected tubing system passed through a mini-pump. In parallel, the cardiovascular parameters were recorded continuously via a computerised finger-cuff sensor. Subjective sexual arousal increased significantly in both men and women during the erotic film, with sexual arousal eliciting an increase in blood pressure in both males and females, and plasma noradrenaline in females only. In contrast, adrenaline, cortisol and prolactin levels were unaffected by sexual arousal. These data further consolidate the role of sympathetic activation in sexual arousal processes. Furthermore, they demonstrate that increases in plasma prolactin during sexual stimulation are orgasm-dependent, suggesting that prolactin may regulate a negative-feedback sexual-satiation mechanism.

Neuropeptide Y (NPY) and endogenous opioids (EOPs) such as methionine-enkephalin (Met-enk) regulate similar physiological responses, but it is not known whether nociceptive and immune responses also show analogy after intracerebroventricular (i.c.v.) application. Dose-response studies show that Met-enk stimulates the blood granulocyte and splenic natural killer (NK) cell function of Lewis rats at a low dose (10(2) ng/kg, i.c.v.), whereas a high dose (10(5) ng/kg) causes suppression of innate immune functions associated with analgesia in the hot-plate test. At 15 min, 1 h and 24 h after i.c.v. application, both Met-enk (10(2) ng/kg) and NPY (1 ng/kg) produced similar effects: An initial suppression of innate immune function was followed by a long lasting stimulatory action on cell functions and serum interleukin-6 (sIL-6) levels. Thus, central NPY application resembles Met-enk-induced immunostimulation at doses not affecting nociception, suggesting an involvement of both peptides in shaping stress-induced immunomodulation of the non-analgetic form, possibly via activation of a common immunomodulatory effector mechanism.

Neuropeptide Y (NPY) alters behavioral activity and innate immune functions of rats within minutes of intracerebroventricular (i.c.v.) application. Using combinations of the Y1-5a,b(6) agonist NPY, the Y1,3,5 agonist [Leu31-Pro34]NPY (LP-NPY), and the selective Y1 antagonist BIBP3226 (BIBP), we investigated whether the NPY-Y1 receptor (Y1R) subtype regulates NPY-induced behavioral and immunological effects at 15 min after i.c.v. application. Administration of both NPY and LP-NPY decreased rearing activity in the open field and suppressed granulocyte function in the blood. These effects were blocked by BIBP pre-treatment. In contrast to the blood, NPY and BIBP+NPY treatments stimulated granulocyte function within the splenic compartment. In addition, a blood leukophilia composed of granulocytes and NK cells was induced by NPY only. We conclude that the tested early effects of NPY are mediated by either the Y1R (rearing, blood granulocyte function), or a non-Y1R (splenic granulocyte function), or by a combined receptor activation (leukocyte mobilization). Furthermore, the immunological effects of NPY demonstrate compartment specificity., (Copyright 1998 Elsevier Science B.V.)