Pathophysiology Of Female Sexual Dysfunction Research Articles

FEMALE SEXUAL DYSFUNCTION WITH DIURETICS IN WOMEN WITH ARTERIAL HYPERTENSION

Objective: Sexual dysfunction is more prevalent in female than in male hypertensive patients. Although the pathophysiology of female sexual dysfunction is more complex than the male one, antihypertensive drugs seem to contribute to female sexual dysfunction. The role of diuretics in female sexual dysfunction remains largely unclarified. We therefore aimed to evaluate the impact of diuretic therapy on female sexual function in hypertensive women free of sexual dysfunction. Design and method: Consecutive female hypertensive patients between 30 and 70 years of age attending our Hypertension Outpatient Clinic who initiated diuretic therapy participated in the study. Female sexual function was evaluated at baseline and three months after diuretic initiation. Female sexual function was assessed using the Female Sexual Function Index, a validated 19-item questionnaire. Results: In total, 218 female hypertensive patients participated in the study. Diuretics were introduced either as monotherapy in patients not taking antihypertensive drugs (58 patients) or as part of combination therapy in patients already taking angiotensin receptor blockers (103 patients) or angiotensin receptor blockers plus calcium antagonists (57 patients). Female sexual dysfunction occurred in 6/58 (10.3%) participants on diuretic monotherapy, in 18/103 (17.4%) participants on dual therapy (ARBs and diuretic addition), and in 9/57 (15.8%) participants on triple therapy (prior ARBs+calcium antagonists and diuretic addition). Conclusions: Initiation of diuretic therapy is associated with incident female sexual dysfunction in 10–20% of women with arterial hypertension. Further studies are needed to verify our findings, enlighten the mediating mechanisms, and clarify the management of such patients.

Cardiometabolic Risk and Female Sexuality-Part I. Risk Factors and Potential Pathophysiological Underpinnings for Female Vasculogenic Sexual Dysfunction Syndromes.

Erectile dysfunction is recognized as an opportunity for preventing cardiovascular (CV) events, and assessing the impairment of penile vascular flow by Doppler ultrasound is an important tool to ascertain CV risk. Conversely, the role of genital vascular impairment in the pathophysiology of female sexual dysfunction (FSD) remains contentious. To focus on the current scientific support for an association between CV risk factors and female sexual health in the 1st part of a 2-part review. A thorough literature search of peer-reviewed publications on the associations between CV risk factors and FSD and their underlying mechanisms was performed using the PubMed database. We present a summary of the evidence from clinical studies and discuss the possible mechanisms providing the pathophysiologic bases of vasculogenic FSD syndromes. The peripheral sexual response in women is a vascular-dependent event, and evidence suggests that cardiometabolic-related perturbations in endothelial function can determine vascular insufficiency in female genital tissues. Although epidemiologic and observational studies demonstrate that the prevalence of FSD is higher in women with diabetes mellitus, a cause-effect relation between these clinical conditions cannot be assumed. Evidence on the effect of obesity, metabolic syndrome, and polycystic ovary syndrome on sexual function in women is controversial. Data on the associations of dyslipidemia and hypertension with FSD are limited. Common cardiometabolic alterations could affect vascular function in the female genital tract. Based on limited data, there is an association between CV risk factors and female sexual health in women; however, this association appears milder than in men. Maseroli E, Scavello I, Vignozzi L. Cardiometabolic Risk and Female Sexuality-Part I. Risk Factors and Potential Pathophysiological Underpinnings for Female Vasculogenic Sexual Dysfunction Syndromes. Sex Med Rev 2018;6:508-524.

Sexual activity in women with cardiovascular disease: a literature review

Female sexual dysfunction (FSD) is a complex condition that involves both psychological and organic domains, including the cardiovascular system, and has an impact on quality of life in more than one third of women. However, only few papers are available in the medical literature regarding FSD and its relation with cardiac diseases. In this review, we discuss the physiology of sexual intercourse in women, the pathophysiology of FSD, the sexual counseling to provide, and the therapeutic choices to minimize the negative impact of cardiovascular diseases on female sexual activity.

The Physiology of Female Sexual Function and the Pathophysiology of Female Sexual Dysfunction (Committee 13A).

The article consists of six sections written by separate authors that review female genital anatomy, the physiology of female sexual function, and the pathophysiology of female sexual dysfunction but excluding hormonal aspects. To review the physiology of female sexual function and the pathophysiology of female sexual dysfunction especially since 2010 and to make specific recommendations according to the Oxford Centre for evidence based medicine (2009) "levels of evidence" wherever relevant. Recommendations were made for particular studies to be undertaken especially in controversial aspects in all six sections of the reviewed topics. Despite numerous laboratory assessments of female sexual function, genital assessments alone appear insufficient to characterise fully the complete sexual response.

MP52-14 EXPRESSIONS OF VAGINAL PHOSPHODIESTERASE 5 AND NITRIC OXIDE SYNTHASE IN FEMALE SEXUAL DYSFUNCTION

You have accessJournal of UrologySexual Function/Dysfunction/Andrology: Basic Research I1 Apr 2015MP52-14 EXPRESSIONS OF VAGINAL PHOSPHODIESTERASE 5 AND NITRIC OXIDE SYNTHASE IN FEMALE SEXUAL DYSFUNCTION Kang Jun Cho, Jang Hwan Kim, Jong Bo Choi, Seung-June Oh, Kyu-Sung Lee, Myung-Soo Choo, Young Ho Kim, and Joon Chul Kim Kang Jun ChoKang Jun Cho More articles by this author , Jang Hwan KimJang Hwan Kim More articles by this author , Jong Bo ChoiJong Bo Choi More articles by this author , Seung-June OhSeung-June Oh More articles by this author , Kyu-Sung LeeKyu-Sung Lee More articles by this author , Myung-Soo ChooMyung-Soo Choo More articles by this author , Young Ho KimYoung Ho Kim More articles by this author , and Joon Chul KimJoon Chul Kim More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2015.02.1731AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Phosphodiesterase 5 (PDE5) and endothelial nitric oxide synthase (eNOS) are important enzymes related to sexual function and are found in the vaginal tissue. We investigated the change in expression of vaginal PDE5 and eNOS in women with sexual dysfunction to identify the pathophysiology of female sexual dysfunction (FSD). METHODS We obtained specimens of vaginal tissue from women aged ≥40 years who were undergoing surgery for stress urinary incontinence and had sexual activity ≥2 times every month for the last 6 months. Those with menopause or histories of vaginal surgery, total hysterectomy, oophorectomy, stage 2 or greater pelvic organ prolapse, diabetes mellitus, depression, and other diseases could influence sexual function were excluded. Patients completed the Female Sexual Function Index (FSFI) questionnaire for the evaluation of female sexual function. The FSD group was defined as patients with an FSFI <18 and arousal domain scores <3. Patients with an FSFI ≥26 and individual domain scores ≥4 were used as a control group. Expressions of PDE5 and eNOS were compared between the FSD and control groups by immunofluorescence staining and Western blotting. RESULTS In total, 16 women were evaluated. The mean total FSFI was 30.8 ± 2.8 in the FSD group (n = 8) and 14.8 ± 2.4 in the control group (n = 8). Immunofluorescence staining showed that PDE5 and eNOS were localized in the vaginal epithelium. In Western blot analysis, immunoreactive bands indicating expression of eNOS were decreased in the FSD group than in the control group, although this was not statistically significant. Immunoreactive bands indicating expression of PDE5 were significantly decreased in the FSD group than in the control group (P = 0.030). CONCLUSIONS eNOS and PDE5 in the vagina have a role in the pathophysiology of FSD. The expression of PDE5 in the vagina was decreased in women with sexual dysfunction. © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e632 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kang Jun Cho More articles by this author Jang Hwan Kim More articles by this author Jong Bo Choi More articles by this author Seung-June Oh More articles by this author Kyu-Sung Lee More articles by this author Myung-Soo Choo More articles by this author Young Ho Kim More articles by this author Joon Chul Kim More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Neurologic Factors in Female Sexual Function and Dysfunction

Sexual dysfunction affects both men and women, involving organic disorders, psychological problems, or both. Overall, the state of our knowledge is less advanced regarding female sexual physiology in comparison with male sexual function. Female sexual dysfunction has received little clinical and basic research attention and remains a largely untapped field in medicine. The epidemiology of female sexual dysfunction is poorly understood because relatively few studies have been done in community settings. In the United States, female sexual dysfunction has been estimated to affect 40% of women in the general population. Among the elderly, however, it has been reported that up to 87% of women complain of sexual dissatisfaction. Several studies have shown that the prevalence of female sexual arousal disorders correlates significantly with increasing age. These studies have shown that sexual arousal and frequency of coitus in the female decreases with increasing age. The pathophysiology of female sexual dysfunction appears more complex than that of males, involving multidimensional hormonal, neurological, vascular, psychological, and interpersonal aspects. Organic female sexual disorders may include a wide variety of vascular, neural, or neurovascular factors that lead to problems with libido, lubrication, and orgasm. However, the precise etiology and mechanistic pathways of age-related female sexual arousal disorders are yet to be determined. In the past two decades, some advances have been made in exploring the basic hemodynamics and neuroregulation of female sexual function and dysfunction in both animal models and in human studies. In this review, we summarize neural regulation of sexual function and neurological causes of sexual dysfunction in women.

The Role of Psychology in the Biologic Pathophysiology of Female Sexual Dysfunction

Historically FSD has been considered to be contextual and based on interpersonal relationships and personal and psychological issues including predisposing factors that may set the stage for later sexual problems like illness or anatomical deformities and early life experiences,precipitating factors that are the immediate triggers for sexual problems such as an unwanted or traumatic sexual experiences, and maintaining factors such as relationship distress or performance anxiety. Recently, however, a primary biologic-based FSD has been shown to occur following use of oral contraceptive pills, associated with SSRI use, occurring following oncologic treatments for gynecologic malignancies such as breast, cervical, uterine or ovarian cancer, and often with tissue atrophy associated with menopause. This lecture will discuss the need for concurrent psychologic and biologic management even though the pathophysiology is primarily biologic. The model for concomitant biologic and psychologic treatment of sexual health problems is modeled after that described by Perelman in the treatment of men with premature ejaculation.

Use of Sildenafil for Female Sexual Dysfunction

To review the pathophysiology of female sexual dysfunction (FSD) and the literature regarding the use of sildenafil in its treatment. Literature was accessed through MEDLINE (1966-April 2006), Iowa Drug Information Service (1966-April 2006), EMBASE (1966-April 2006), and bibliographies of pertinent articles. Search terms included female sexual dysfunction; sexual dysfunction, psychological; phosphodiesterase inhibitors; and sildenafil. The lack of a clear understanding of FSD contributes to the limited treatment options available. Studies regarding the safety and efficacy of the phosphodiesterase 5 inhibitor sildenafil in the management of FSD were evaluated. Many trials have been of poor quality, making clinical application of their results difficult. The current literature does not show sildenafil to be an effective treatment option for FSD. Treatment of FSD should include both physical and psychological components. Based on the limited data available, it appears that sildenafil, while well tolerated, offers little or no benefit to most patients with FSD.

Physiology of female sexual function and dysfunction

Female sexual dysfunction is age-related, progressive, and highly prevalent, affecting 30-50% of American women. While there are emotional and relational elements to female sexual function and response, female sexual dysfunction can occur secondary to medical problems and have an organic basis. This paper addresses anatomy and physiology of normal female sexual function as well as the pathophysiology of female sexual dysfunction. Although the female sexual response is inherently difficult to evaluate in the clinical setting, a variety of instruments have been developed for assessing subjective measures of sexual arousal and function. Objective measurements used in conjunction with the subjective assessment help diagnose potential physiologic/organic abnormalities. Therapeutic options for the treatment of female sexual dysfunction, including hormonal, and pharmacological, are also addressed.

Biological and Psychosocial Pathophysiology of Female Sexual Dysfunction During the Menopausal Transition

Although increasing age is a primary determinant of reduced sexual function in older women, hormonal changes may be significant contributors to female (and couples') sexual dysfunction. To analyze the most relevant biological, psychosexual, and/or contextual factors that influence changes in women's sexuality during and after menopause. A Postmenopausal FSD Roundtable consisting of multidisciplinary international experts was convened to review specific issues related to postmenopausal women and sexual dysfunction. Expert opinion was based on a review of evidence-based medical literature, presentation, and internal discussion. Menopause is associated with physiological and psychological changes that influence sexuality: the primary biological change is a decrease in circulating estrogen levels. Estrogen deficiency initially accounts for irregular menstruation and diminished vaginal lubrication. Continual estrogen loss is associated with changes in the vascular, muscular, and urogenital systems, and also alterations in mood, sleep, and cognitive functioning, influencing sexual function both directly and indirectly. The age-dependent decline in testosterone and androgen function, starting in the early 20s, may precipitate or exacerbate aspects of female sexual dysfunction; these effects are most pronounced following bilateral ovariectomy and consequent loss of 50% or more total testosterone. The contribution of progestogens to sexual health and variability in the effects of specific progestogens are being increasingly appreciated. Comorbidities, influenced by loss of sexual hormones, between mood and desire disorders and urogenital and sexual pain disorders are common and remain frequently overlooked in clinical practice. Physical and psychosexual changes may contribute to lower self-esteem, and diminished sexual responsiveness and sexual desire. Nonhormonal factors that affect sexuality are health status and current medication use, changes in or dissatisfaction with partner, partner's health and/or sexual problems, and socioeconomic status. Determination of the best way to provide optimal management of sexual dysfunction associated with menopause requires additional controlled studies.

Blood pressure produces deleterious effects in genital structures of female spontanously hypertensive rat

Emerging knowledge from clinical and experimental studies provides a new insight for understanding the pathophysiology of female sexual dysfunction in patients with arterial hypertension. The aim of the present study was to evaluate possible morphological alteration in clitoris and vagina from spontaneous hypertensive rats (SHR) and compared with normotensive Wistar-Kyoto (WKY) rats. Twelve-week-old female SHR and WKY rats, were studied during six months. G1 Control WKY (n = 10) and G2 SHR (n = 10). Systolic blood pressure (SBP) was recorded monthly. At end of the experiment, clitoris and vagina were dissected out and processed by Masson's trichrome, monoclonal anti-a-smooth-muscle actin, anti- collagen type I and type III, and anti TGFb1. Histomorphometric evaluation revealed that SHR presented higher amount of clitoral cavernous smooth muscle (20 ± 6.9 % versus 7 ± 4.4 %; p< 0.01), as well as vascular smooth muscle (16.1 ± 3.6 % versus 9 ± 2 %; p< 0.01); higher TGFb1 in clitoral vessel wall (2.7 ± 1.4 % versus 1.4 ± 0.5 %; p< 0.01); higher wall/lumen ratio (p< 0.01) in both vaginal and clitoral vessels; and remarkable interstitial fibrosis (60.7 ± 4.9 % versus 38.6 ± 2.7 %; p< 0.01), expressed by a higher amount in interstitial collagen type III and I (p< 0.01) in both clitoris and vagina, when compared to WKY rats. In addition, nerve fibers from clitoral and vaginal tissue in SHR showed a notable fibrosis at perineurium and endoneurium. SHR showed positive correlation between SBP and clitoral cavernous smooth muscle (r= 0.87 p< 0.01); SBP and fibrosis in clitoris (r= 0.81 p< 0.01); and SBP and collagen type I and III (r= 0.92 p< 0.01; r= 0.84 p< 0.01) in clitoris respectively: Similar findings were observed between SBP and collagen type I and III in vagina (r= 0.68 p< 0.05; r= 0.75 p< 0.05). According to these results we conclude that SHR present morphologic changes in clitoral vessels as well as in clitoral cavernous space, which have a high positive correlation with the high blood pressure level. Moreover, the increase in extracellular matrix expansion affects not only the clitoral and vaginal interstitium but also the nerve structures from both clitoris and vagina.

Physiology and pathophysiology of female sexual function and dysfunction.

Female sexual dysfunction is age-related, progressive, and highly prevalent, affecting 30%-50% of American women. While there are emotional and relational elements to female sexual function and response, female sexual dysfunction can occur secondary to medical problems and have an organic basis. This paper addresses the anatomy and physiology of normal female sexual function as well as the pathophysiology of female sexual dysfunction. Although the female sexual response is inherently difficult to evaluate in the clinical setting, a variety of instruments have been developed to assess subjective measures of sexual arousal and function. Objective measurements, used in conjunction with the subjective assessment, help diagnose potential physiologic/organic abnormalities. Therapeutic options for the treatment of female sexual dysfunction, including hormonal, and pharmacological, are also addressed.