To assess the contribution of gonadal steroids to sexual behavior in aging women, we conducted a 10-week, double-blind, hormone replacement study of 40 naturally menopausal women (mean age, 58.3 yr). Prospective measurements of basal and stimulated vaginal vasocongestion and daily self-reports of mood, physical symptoms, sexual behavior, and perceived sexual pleasure were collected. Daily treatments were either conjugated equine estrogen, i.e. Premarin (P; 0.625 mg), Premarin and medroxyprogesterone acetate, i.e. Provera (PP; 0.625 and 5 mg, respectively), Premarin and methyltestosterone (PT; 0.625 and 5 mg, respectively), or placebo (PL). Compared to placebo, hormone treatment had significantly reduced hot flashes in the P and PP groups by week 4 and in the PT group by week 5. Headaches were reduced in the P vs. PL group, only. Hormone treatment did not significantly alter mood ratings, sexual behaviors, or psychophysiologically measured sexual arousal. PT treatment significantly increased reports of pleasure from masturbation compared to the other three groups, underscoring the apparent contribution of androgens to self-stimulatory behavior. However, the data suggest that in these physically and sexually healthy women, gonadal steroids do not influence major components of sexual functioning, including arousal and a wide variety of sexual activity and experience.

To investigate the possible role of sensory function in conditions affecting sexual function, sensory thresholds were compared between young healthy men (n = 14, means age = 29.8), aging men (n = 15, means age = 67.3), and men suffering from diabetic impotence (n = 15, means age = 45.0). Using the psychophysical method of forced choice, vibrotactile and electrical stimulation thresholds were deterlmined in two separate sessions at two body sites: the fingertip and the ventral surface of the penis, just proximal to the glans. Vibrotactile penile thresholds (VTP) were lowest for young (Y) subjects and much higher for both aging (A) and diabetic (D) subjects. Electrical stimulation of the penis (ESP) showed the same trends, although the differences only approached significance (p = 0.06). The vibrotactile finger threshold (VTF) was significantly higher for A subjects as compared with Y and D subjects, but there was no difference between the Y and D groups. Diabetic patients had significantly higher thresholds for electrical stimulation of the finger (ESF), in contrast to the VTF finding. Finger thresholds were significantly lower than penile thresholds for all groups, and the change in threshold from finger to penis was greater in both aging and diabetic than in young subjects. Age was positively correlated with thresholds for ESF, ESP, VTF, and marginally for VTP when all three groups were analyzed together. However, in general the results of threshold determinations could not be attributed merely to age. Based on a detailed questionnaire of sexuality, VTP was negatively correlated with sexual activity and both ESP and VTP were negatively correlated with erectile capacity. The data are consistent with a genital sensory role for age-related and diabetic changes in sexual function.

Twenty premenopausal, 14 postmenopausal, and 14 postmenopausal women receiving replacement estrogen therapy were studied to determine whether differences in hormone status were associated with differences in physiological and subjective sexual responses. All subjects viewed a neutral, an erotic, and a second neutral videotape while photoplethysmographic vaginal pulse amplitude was continuously recorded. Self‐report ratings of sexual arousal and affective response were collected. Serum levels of testosterone, estradiol, estrone, and luteinizing hormone were obtained. The three groups did not differ in either average or maximum vaginal pulse amplitude to the videotapes nor in latency of sexual response. The postmenopausal women not taking replacement estrogen reported significantly less vaginal lubrication in response to the erotic videotape than the higher estrogen premenopausal and replacement hormone groups. Estradiol level was significantly correlated with ratings of vaginal lubrication in response to the erotic videotape but not with vaginal pulse amplitude. Results thus suggest that estrogen is important in maintaining vaginal lubrication and the perception of sexual arousal but not in determining vaginal vasocongestion.

The present experiments were performed to test the hypothesis that, in vivo, intrapituitary angiotensin II (ANG II) mediates the effect of luteinizing hormone-releasing hormone (LHRH) on prolactin release. After intravenous administration of LHRH (100 ng/100 microliters saline), plasma levels of both luteinizing hormone (LH) and prolactin were increased in ovariectomized rats pretreated with estradiol and progesterone. Intravenous administration of saralasin or sarthran (ANG II receptor blockers) reduced or abolished, respectively, the LHRH-induced increase in prolactin without affecting the rise in LH. In other ovariectomized steroid-treated rats, saralasin did not affect the increase in LH or prolactin induced by 10 min of restraint stress. Finally, in intact female rats on the day of proestrus, neither saralasin nor sarthran affected the mid-cycle prolactin surge. Taken together, these results show that in vivo exogenous LHRH stimulates prolactin release via a paracrine action of pituitary ANG II. However, under other conditions in which both LH and prolactin (and presumably endogenous LHRH) are elevated, pituitary ANG II does not appear to be involved in the prolactin rise.

This study was designed to investigate the effects of exogenous and endogenous angiotensin II (All) on prolactin release in ovariectomized rats, with and without estrogen and progesterone pretreatment. In the first series of experiments, All or vehicle was injected into the third cerebral ventricle of conscious, freely-moving rats. In both treated and untreated rats, administration of 50 ng All suppressed prolactin levels within 15 min of injection, compared to vehicle-injected rats. In untreated rats, prolactin levels returned to baseline values by 30 min, while in treated rats, prolactin levels remained suppressed for an hour.In the second series of experiments, the involvement of endogenous brain All in tonically suppressing prolactin release was assessed by administering either All receptor blockers (saralasin or sarthran) or an All synthesis inhibitor (enalaprilat, an inhibitor of the conversion of angiotensin I to All). Neither All receptor blockade nor converting enzyme inhibition resulted in any change in prolactin levels in untreated levels in untreated rats. However, following treatment with ovarian steroids, infusion of saralasin or injection of enalaprilat resulted in a significant increase in plasma prolactin titers. During saralasin infusion, prolactin levels were significantly increased by 15 min and continued to be higher than controls at 60 min. After enalaprilat administration, prolactin levels did not rise significantly until 90 min and then remained elevated up to 120 min post-injection. These latter results suggest that at least one h is required for maximal inhibition of angiotensin synthesis in the brain.These data demonstrate that low doses of All suppressed basal prolactin secretion in both untreated and ovarian steroid-treated, ovariectomized rats. However, treated rats appeared to be more sensitive than untreated animals to the prolactin-lowering effects of centrally administered All. The lack of prolactin response in untreated rats when brain All synthesis was inhibited or All receptors were blocked suggests that, in the absence of ovarian steroids, endogenous All was not acting tonically to suppress prolactin secretion. Following exposure to ovarian steroids, however, the endogenous brain All system appeared to be activated and involved in controlling prolactin release.The anterior pituitary gland hormone, prolactin, i s involved in lactation, ovarian and mammillary gland function, pseudopregnancy in female rats, and i s released in response to stress (1). In human males and females, hyperprolactinemia i s associated with impaired sexual behavior and functioning, as well as infertility (2).Prolactin secretion is mainly under tonic inhibitory control by dopamine, derived from the brain tuberoinfundibular system (3). On the other hand, a variety o f peptides (e.g. vasoactive intestinal peptide, thyrotropin-releasing hormone) including angiotensin I1 (AII), have been identified as putative prolactin-releasing factors when applied directly to the anterior pituitary gland (4). Und...