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European Urology


European Urology 47 (2005) 838–845

Erectile Dysfunction and Lower UrinaryT ract Symptoms Secondary to BPH
Kevin T. McVary*
Department of Urology, Feinberg School of Medicine, Northwestern University Medical School, Tarry 16-749, 303 E. Chicago Ave., Chicago, IL 60611, USA Accepted 8 February 2005 Available online 16 March 2005

Abstract Introduction: The relationship between lower urinary tract symptoms (LUTS) and erectile dysfunction (ED) have received increased attention recently because both diseases are highly prevalent, frequently co-associate in the same aging male group, and contribute significantly to the overall quality of life. The association between these two diseases has also garnered attention as investigators have hypothesized a common pathophysiology to explain the assertion that they are causally linked. Methods: A causal association between LUTS and ED cannot be established on the basis of the ever-increasing number of epidemiological studies. Attempting to explain a causal relationship between ED and LUTS needs to be examined using Hill’s criterion, which is used by many epidemiologists to separate causal from non-causal explanations. Results: Given the epidemiological components of the Hill’s Causality method, it is clear that there is a strong strength of association, internal consistency, and dose response effects between ED and LUTS. Because of the strong cross-sectional flavor to the epidemiological studies, the temporal relationships between ED and LUTS remain unknown. The issue of an ‘‘alternate explanation’’ to describe the LUTS-ED association appears to be accounted for in that several large studies have provided convincing multiple regression analyses in which the ED-LUTS relationship remains significant. The link between ED and LUTS has biologic plausibility given the four leading theories of how these diseases interrelate. These explanations fall into four theories each with a variable amount of supporting data. These include: (1) NOS/NO levels decreased or altered in the prostate and penile smooth muscle, (2) Autonomic hyperactivity effects on LUTS, prostate growth and ED., (3) increased Rho-kinase activation/endothelin activity, and (4) prostate and penile ischemia. Conclusions: LUTS and sexual dysfunction are highly prevalent in aging men. Both conditions are also significant contributors to overall quality of life. New data has emerged to indicate potential links in epidemiological, physiologic, pathophysiologic and treatment aspects of these two entities. # 2005 Elsevier B.V. All rights reserved. Keywords: BPH; LUTS; Erectile dysfunction; ED; Prostate; Penis; Autonomic hyperactivity

1. Introduction The relationship between lower urinary tract symptoms (LUTS) and erectile dysfunction (ED) have
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received increased attention recently because both diseases are highly prevalent, frequently co-associate in the same aging male group, and contribute significantly to the overall quality of life. The association between these two diseases has also garnered attention as investigators have hypothesized a common pathophysiology to explain the assertion that they are cau-

0302-2838/$ – see front matter # 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.eururo.2005.02.001

.2%. the Krimpen study of sexual dysfunction assessed the relative risk (RR) for ED in a community cohort [11].3–14. Compared to men in their 40s. An early cross-sectional investigation of the role between sexual function and LUTS using a community-based survey noted sexual satisfaction negatively correlated with increasing age and LUTS [9].2].e.5 2. between study consistency (replication of findings). Epidemiology of LUTS secondary to BPH and sexual dysfunction Before looking at the relationship between LUTS and ED. as well as the more standard risks of hypertension. alpha-blockers and PDE-5 inhibitors) that need special attention when dealing with any man with ED or LUTS.8 to 7. Similarly.3 3. The Hill ‘‘causality method’’ establishes a link using general epidemiological data.3 fold increase in relative risk for symptom scores greater than 19.0 to a 3. The Massachusetts Male aging Study (MMAS) detailed that 52% of men from 40–70 years old have some degree of ED. This suggests that ED is a worthwhile symptom to query in patients who present with LUTS. The epidemiological data is examined for the strength of association (relative risk [RR].3– 53. and cohort studies grounded by supportive plausible mechanism of action investigations. potentially clinically significant BPH lesions shares this association with increasing age. which is used by many epidemiologists to separate causal from non-causal explanations [1. there are relevant clinical management questions related to their common association. bias and confounding factors). Age is one of the most important risk factors for ED. Using a community based survey of over 4000 men the ‘Cologne Male Survey’ noted the prevalence of ED was 19. diabetes. Thus.9 1. the observed epidemiological data must take into consideration alternative explanations (i. even if BPH/ LUTS and ED were simply coincidental. Given the potential role of bladder and CNS roles in LUTS this seemingly surprising anomaly of women with LUTS does not impact the putative relationship between ED and LUTS. the prevalence of histologic BPH increases progressively from the fourth (8%) through the eighth (82%) decade [5]. case-control reports. The prevalence of gross. men in their 50s have a 2-fold increase in their relative risk of ED. 2.5 1. The cumulative prevalence of a history/physical examination based diagnosis of LUTS or BPH voiding dysfunction similarly increased progressively from 26% to 79% from the 5th to 8th decade of life in the Baltimore Longitudinal Study of 1057 men [6]. The link between ED and LUTS is also important for physicians to understand because the treatment of one may adversely impact the other disease. Almost all accepted therapies for LUTS (surgical or medical) can impact some aspect of sexual health.. chance.T. In this important study LUTS had a strong relationship with increasing risk of ED (dose response curve). An unequivocal role for BPH in the LUTS data should be viewed with some reservation as several studies have documented a comparable prevalence of similar symptoms in aging women [7. The authors noted an increased RR of ED from 1. This ‘‘common-theme’’ hypothesis has taken a life of its own as pharmaceutical companies have contemplated expanding indications for their drugs for both diseases. and pelvic surgery [10]. a brief overview of the prevalence of LUTS and ED is worthwhile. Similar to ED.4%) and a high co-morbidity of ED with LUTS. The relative risk of ED stratified by International Prostate Symptom Score (IPSS) ranged from 0 at relative risk 1. and 2/3 of these men have moderate to severe symptoms [4]. This association of ED with LUTS was also confirmed in several more recent cross sectional commuTable 1 Risk Factors for Erectile Dysfunction (Krimpen Study) Blanker 2001 Age (55–78) BMI >30 LUTS Cardiac Sx COPD Smoking 2. thus it is imperative that health care professionals understand their patients concerns and motivations in these two linked diseases. with a steep age-related increase (2. pulmonary problems and a history of smoking (Table 1).K.8–7. This increased RR of ED based on the severity of LUTS was greater than that found with the more traditional ED risk factors (cardiac symptoms.0 1.8].6 The large variation in LUTS related Ed risk relates to the severity of the IPSS score (adapted from: [11]). McVary / European Urology 47 (2005) 838–845 839 sally linked. Most importantly. there are important specific drug interaction issues (e.5 depending upon the degree of urinary complaints. This increases to 5-fold increase in RR for men in their 60s [3].g. dose-response effect and a temporal relationship between index disease development and progression. Additionally. Attempting to explain a causal relationship between ED and LUTS needs to be examined using Hill’s criterion. A causal association between LUTS and ED cannot be established on the basis of the ever-increasing number of epidemiological studies.

The Multinational Survey of the Aging Male (MSAM-7) study revealed a strong association between the level of sexual activity and IIEF score with patients’ IPSS score [14] (Fig. Importantly. problem assessment. 3. who noted that ED and reduced ejaculation were highly prevalent in men with LUTS and was strongly related to increasing age and LUTS severity [18]. Age and LUTS severity stratification of erectile dysfunction in the MSAM-7 Study. ejaculatory function. or LUTS were significantly (p < 0. The bothersomeness of SD in the aging male was confirmed by Vallancien et al. Moreira et al. In a population-based household survey. and dose response effects (worse LUTS-worse ED) between ED and LUTS. The results of the MSAM-7 suggest that older men still have an active sex life and that the severity of LUTS has an impact on sexual disorders independent of other risk factors. and overall sexual satisfaction were significantly and inversely correlated with LUTS [13]. Of note. The authors noted that sexual drive. Because of the strong crosssectional flavor to the epidemiological studies. problem assessment and the overall satisfaction of sexual life (p < 0. lipid disorders. A secondary aim of this important study addressed the relationship between sexual function and LUTS severity in 3. and overall satisfaction with sexual life (p < 0. and diabetes) were controlled in a multivariate analysis and the patients were characterized clinically exceedingly well. depression.3%).1%. Additionally. internal consistency. Note the increasingly common incidence of ED per each age group (50–59. Fig. it is clear that there is a strong strength of association. problem assessment. noted an age-adjusted prevalence of ED of 39. 1. 70–79 years). Evaluating the relationship between ED and LUTS was done in the context of the Olmstead County Study of LUTS. partner status. It is well known that LUTS diminishes the quality of patients’ life. The NIH-sponsored MTOPS trial addressing the effect of finasteride and/or doxazosin on BPH progression was recently reported [15]. if there is link between ED and LUTS from the epidemiological standpoint then this . Given the epidemiological components of the Hill’s causality method mentioned earlier. this association between LUTS and ED persisted when controlled for age and other co-morbidities that are known to impact sexual function. Within in age group there is an impressive variation in ED as stratified by LUTS severity (IPSS score).001 for each domain) [16]. Other measures of ejaculatory dysfunction. 60–69. Looking at the prevalence of SD and LUTS in a crosssectional analysis of baseline data. McVary / European Urology 47 (2005) 838–845 nity-based populations.001). total prostate volume.T. hypertension.. The relationship between Qmax. diabetes.01). McVary reported a strong association between baseline AUA Symptom Index and the various domains of sexual function includ- ing libido. reduced ejaculate and ejaculation pain also strongly associated with LUTS. There was also significant association of the sexual function domains and maximum flow rate (Qmax) (p < 0.05) associated with increased prevalence [12].1%. (Adapted from: [14]). sexual satisfaction also significantly associates with LUTS in that the more severe the LUTS. moderate 13. the temporal relationships between ED and LUTS remain unknown. Mechanism of interaction between ED and LUTS As mentioned above. ejaculation. Girman and colleagues demonstrated a similar relationship between prostate volume and sexual dissatisfaction [17].000 men.5% (minimal 25. transition zone volume and ED noted in the MTOPS is important as it links the symptoms of ED with more fundamental biologic and physiologic measures of prostate and bladder dysfunction. erectile function.840 K. the duration of LUTS associated very strongly with erectile function. erectile capability. This study is most interesting because of the association of prostate volume (as a proxy for basic biologic growth principles) and sexual dysfunction. In a follow-up report. the more likely a poor sexual satisfaction was reported. Having never been married. The issue of an ‘‘alternate explanation’’ to describe the LUTS-ED association appears to be accounted for in that several large studies have provided convincing multiple regression analyses in which the ED-LUTS relationship remains significant. These results support the association of LUTS and SD that is independent of the usual co-morbidities. This latest report is also important because the co-morbidities that are frequently associated with ED (including age. 1). marital status. severe 1.

The functional relevance of these PDE isoenzymes is noted in the relaxing effect of nonspe- Fig. which then reduces prostatic tone relaxation. NOS/NO levels decreased or altered in the prostate and penile smooth muscle This hypothesis attempts to explain the link between ED and LUTS by the reduced production of nitric oxide synthase (NOS)/nitric oxide (NO) in the pelvis. The physiologic role of NOS/NO is not well characterized in the prostate. This theory is supported by limited evidence in which BPH tissue NADPH-d staining and nNOS immunohistochemistry shows a qualitative decrease in the otherwise dense nitrinergic innervation of glandular epithelium. or as part of normal compliance. Human (n = 12) and canine (n = 8) prostatic tissue strips were exposed to sodium nitroprusside. It links these two diseases into a single unifying concept as it is reported that NOS/NO production of the prostate is reduced in BPH (transition zone) when compared to normal prostate tissue. Proposed theory of pelvic loss of nitric oxide synthase (NOS) and nitric oxide (NO). For a reduction of NOS/NO to explain a role in LUTS. each with a variable amount of supporting data. [25].1. Sodium nitroprusside elicited a relaxation response relative to baseline tension. give credence to this theory [24]. and the act of urination. This data. 3. It logically follows that prostate tissue levels of NO/ NOS are reduced in BPH progression. 3. and blood vessels. The steady reduction of nNOS gene expression with increased age in adult rat prostates supports the biologic plausibility of this theory [22]. Additionally. Results expressed as mean grams per square centimeter crosssectional area ÆSE. combined with in vitro models that demonstrate an anti-proliferative effect on human prostatic smooth muscle cells by NO donors (nitroprussideSNP). and a negative effect on the proliferation signal transduction pathway (protein kinase C) with SNP. which includes both the penis and prostate [19] (Fig. . a NOS-mediated prostatic smooth muscle relaxation must occur at a critical point in the voiding reflex. Given that this hypothesis is based on a limited number of studies that depend largely on descriptive immunohistochemistry and Rt-PCR measures of gene expression. Reduction of NOS/NO from various systemic disease results in increased smooth muscle cell (SMC) contractile forces at the bladder neck and prostatic urethra. Increase in prostatic smooth muscle relaxation when exposed to NO donors. fibromuscular stroma. Both forces result in the worsening of LUTS (adapted from: [19]). Fig.21]. There are several methodological flaws with this data but the concept does have a consistent appeal [20. 2). an exogenous source of nitric oxide. This proposed reduction in NOS isoforms results in an altered neurogenic influence on voiding function that is recognized as progressive BPH or LUTS. 2. evidence for a NOS role in voiding is currently lacking. the reduced NOS/NO results in prostatic smooth muscle cell proliferation and increased outlet resistance. increased cell proliferation with NO antagonists. the bladder. 3). Circumstantial evidence in human and canine organ chamber studies demonstrating prostatic smooth muscle relaxation with exposure to NO donors only goes part way in explaining the role of NOS in LUTS with normal or dysfunctional voiding [23] (Fig. What are the possible biologic interrelationships between these two entities? These explanations fall into 4 categories or theories. The LUTS-ED:NOS/NO theory is further supported by the characterization and functional relevance of cyclic nucleotide phosphodiesterase (PDE) isoenzymes of the human prostate. McVary / European Urology 47 (2005) 838–845 841 relationship must have biologic plausibility. The most common PDEs noted in prostate tissue were PDE-type 4 and PDE-type 5. This theory closely adheres to the nitrinergic innervation-smooth muscle cell relaxation molecular mechanism of ED.T. (Adapted from: [23]).K.

The ANS is well known to be intimately involved in the mechanisms of voiding. McVary / European Urology 47 (2005) 838–845 cific PDE inhibitors (papaverine) as well the effect of specific PDE inhibitors (sildenafil).e. Type 11A protein abundance was greatest in the prostate compared to the other these organs.e. (Adapted from: [34. Clearly. increased age. they also noted that treatment with sildenafil appeared to improve urinary symptom scores. Autonomic hyperactivity and metabolic syndrome effects on LUTS.2.T. The improvement in erectile function noted in this model. ED and BPH progression. We recently reported the quantitative relation between ANS tone and the subjective experience of dysfunctional voiding [34]. Limited pilot studies demonstrating an impact of sildenafil on both ED and LUTS supports the NOS/NO theory. prostate hyperplasia and erectile dysfunction [30–32]. This increased sympathetic tone effects BPH growth. prostate growth and ED Our lab first identified the autonomic nervous systems (ANS) control of prostate growth and differentiation. lack of blinding or other unrecognized factors is not known. it is very possible that hyperactivity of the ANS could adversely impact LUTS and erectile function. Autonomic hyperactivity.19]). Most interesting.’’ Whether this lack of relationship relates to the modest sample size. Proposed theory of autonomic hyperactivity of LUTS and ED. 3. 4). Also. Hopps et al. or increased ANS activity.g. and the prostate [26]. Our recent evidence has shown that ANS hyperactivity is significantly associated with the most commonly employed measures of LUTS (AUA symptom score and BPH Impact Index score). It remains unclear whether the increase in LUTS or ED is the result of a central increase in sensitivity to peripheral signals. or metabolic syndrome. The authors reported ‘‘no relationship between ED and LUTS. fear leads to dry mouth and tachycardia). explanation is attractive because it links established clinical physiologic findings of LUTS. The autonomic hyperactivity. or a consequence of an alteration in the function of the bladder/penis itself that generates increased central activation. a well-designed and controlled study is mandatory to further elucidate the relationship between these two important diseases. but enthusiasm must be tempered by the open-label noncontrolled nature of these single centered studies. the magnitude of increase in serum NE after provocative neurologic stress (tilt test) significantly correlates with prostate . Although this pilot study was not blinded or placebo controlled. and decreased physical activity. Given that ANS translates ‘‘mood’’ into objective physiology (e. it does suggest a common mechanism and/or therapy for this LUTS-ED symptom complex. Investigators treating patients with both ED and LUTS using sildenafil noted a lower IPSS.842 K. Increased autonomic hyperactivity resulting from increased BMI. after brief aggressive treatment of the hypertension. In a similar vein. in which Northern and RNA dot blots for PDE11A gene expression noted its presence in testes. The role of prostatic PDE11A is unknown. hyperinsulinemia. 4. skeletal muscle. Several studies have attempted to assess the relationship between ED and LUTS by treating one symptom (i. Those with a lower IPSS at baseline had a better response to ED therapy [27]. BPH and ED with established basic science evidence [19] (Fig. These findings were supported by additional animal studies using a strain of rats (spontaneously hypertensive rats-SHR) that develop increased autonomic activity. The concept that PDE-5 inhibitors could be utilized to improve LUTS is provocative. The various animal models suggesting a role between autonomic nervous system (ANS) overactivity and increased prostate growth is further supported by epidemiological investigations linking the clinical diagnosis of BPH with increased autonomic tone [33]. This has implications for understanding the pathophysiology of BPH. The ANS provides an environment that induces rat prostatic growth while its absence results in regression of the gland [29]. prostate growth. LUTS and vasocontrictive forces that results in ED. reported mild improvements in LUTS when treated with on-demand PDE-5 therapy (sildenafil) for ED in men with concomitant LUTS [28]. Of more interest to this study is the recognition by Fawcett et al. is significantly associated with the signs and symptoms of BPH. but its relatively low abundance in the smooth muscle makes its pivotal role in the LUTS-ED relationship less likely. resistance within the penis and the decrease in responsiveness of alpha1-adrenoceptor mediated erectolytic signaling. ED) and measuring the impact on the other disease (i. may be related to improvement in structurally based vascular Fig. LUTS).

Impact on erectile dysfunction of alpha-blockers If LUTS and ED are causally linked. The suggestion that BOO induces ED via an upregulation of Rho kinase in the penis has experimental merit. 4. Understanding how this Fig.001). This theory is compatible with other proposed theories (NOS/NO. Similarly. Chang et al.4. (Fig. physical inactivity and age). The risk factors for ED impact pelvic arterial blood flow resulting in loss of smooth muscle from bladder. insulin level. detrusor and resultant in loss of bladder compliance.) as pelvic ischemia may induce ANS hyperactivity. penis and bladder [37]. mood related factors. 4). a1blockers with excessive hypotensive effects may be anti-erectile by reducing penile filling pressure. reported that corpus cavernosum SM from rabbits with partial bladder outlet obstruction showed a broad range of molecular and functional differences versus controls. 5. smoking. The relevant mechanism explaining the bladder effects may be very similar to those associated with bladder ischemia (bladder outlet obstruction or pelvic vascular disease) inducing the same SM loss with replacement of collagen deposition and fibrosis as well as loss of compliance. This modulation of LUTS and ED works under the influence of central. autonomic hyperactivity or increased sympathetic tone is a known regulator of SM relaxation and penile reactivity. What is the impact on erectile function when patients are treated with alpha-blockers? Alpha-blockers might contribute to the improvement of ED by altering the balance of penile vasoconstrictive and vasorelaxant forces in favor of the proerectile mechanisms. could adversely effect penile SM function is consistent with our current understanding of the penile pro-erectile response. hypercholesterolemia and diabetes mellitus) also impacts LUTS and BPH.3. On the contrary. Animal models mimicking pelvic ischemia and hypercholesterolemia show a striking similarity in the smooth muscle alterations of the detrusor and corpora. Although not entirely clear whether this putative mechanism is causative or even exclusive of the abovementioned possibilities. There is also a possibility that a multisystem dysfunction of Rho kinase exists and leads to both ED and LUTS. Oral a-receptor antagonists exert their effects by blocking the actions of norepinephrine at a1-adrenoceptors on cavernosal smooth muscle cells. The relationship between ANS hyperactivity and LUTS still persists after controlling for extrinsic influences on ANS activity (BMI. 5).T. etc. These findings may have important implications concerning the pathophysiological mechanisms underlying or influencing LUTS and ED (Fig. reduce NOS expression. decreased innervation and increased smooth muscle bundle size [35]. McVary / European Urology 47 (2005) 838–845 843 size (p < 0. hyperactivity and impaired contractility. A similar process occurring in the penis results in smooth muscle loss in the penis with resultant ED. These changes include increased penile SMC contractility. 3. then treatment of LUTS with alpha-blockers may improve ED. its inclusion here is well justified. The proponent theorized that the risks for ED (hypertension. This is supported by evidence of Rho kinase dysfunction in the bladder following BOO [36]. At the same time there is an effect on prostate fibrosis with resultant increase in urethral resistance. and upregulate Rho kinase. and modest alterations in total SM myosin. 3. reduced relaxation. This results in LUTS. including hypoxia-induced over-expression of TGFb1 and altered prostanoid production. metabolic syndrome. There are several potential mechanisms for this.K. Pelvic atherosclerosis as a mechanism for LUTS and ED An additional hypothesis causatively linking ED and LUTS is diffuse atherosclerosis of prostate. Norepinephrine released from sympathetic nerve terminals ordinarily acts at postjunctional a1-receptors to produce smooth muscle . (Adapted from: [37]). The autonomic hyperactivity theory of LUTS proposes that the ANS acts as a modulator of voiding symptoms and/or ED about their anatomically or physiologically designated baseline. Alternate Pathway mechanism: Rho-kinase activation/endothelin activity Several investigators have suggested that the socalled ‘‘Alternate Pathways’’ of SM relaxation and contraction may be responsible for the relationship between ED and bladder outlet obstruction (BOO) [19].

If the association between ED and LUTS was causally related. With the exception of tamsulosin. Smoking and erectile dysfunction: evidence based analysis. the effect of a once a day. 22 (57. prostate growth and ED. US Department of Health and Human Services. MD.14(Suppl. These include: (1) NOS/NO levels decreased or altered in the prostate and penile smooth muscle. Carrier S. McVary / European Urology 47 (2005) 838–845 contraction and detumescence. thus suggesting a common etiology or mechanism. Goldstein I. flow rates and prostate volume further supports this relationship.. Wessells H.17:241. The synergistic effects of vascular dilation and blockade of sympathetic inhibition is one explanation for this response [41].151(1): 54–61.0). [6] Guess HM. There are numerous publications within the past 10 years based on sophisticated community and clinical based data suggesting a strong and consistent association between LUTS and ED. Cumulative prevalence of prostatism matches the autopsy prevalence of benign prostatic hyperplasia. (3) increased Rho-kinase activation/endothelin activity. A significant association between LUTS. It is not likely that the alphablockers used for LUTS would affect the presynaptic a2receptors given the selectivity profile [38]. The association is supported by the consistent linear relationship of more severe LUTS with more severe ED. Both conditions are also significant contributors to overall quality of life. Arrighi HM. 1):S29–34. Improvement was most marked in those with the most severe LUTS.001). . physiologic. There are few reports detailing the impact of alpha-blocker use on ED improvement. ED) and measuring the impact on the other disease (i. and is a likely candidate for a mechanism of action in the autonomic hyperactivity model. why should urologists worry about SD in men with LUTS in the first place? This relationship is important because (1) additional information on risk factors for either disease could be important for patient screening. DHHS (PHS) 84-50204. Overall. The development of human benign prostatic hyperplasia with age.9(2. [4] Feldman HA. and (4) prostate and penile ischemia. investigated the synergistic effects of doxazosin and intra-cavernosal therapy (ICI) in those for whom ICI alone failed to induce an erection. (3) sexual problems related to LUTS are not necessarily limited to ED and (4) many currently available LUTS treatments (medical and surgical) affect sexual function. et al. Several studies have attempted to assess the relationship between ED and LUTS by treating one symptom (i.844 K. sexual satisfaction. The patient bother attributable to this affect is less clear. The health consequences of smoking – Cardiovascular disease–A report of the surgeon general. J Urol 2001. New data has emerged to indicate potential links in epidemiological. Because the addition of alpha-blockers may have a beneficial effect in patients with ED. Lukacs et al. Hatzichristou DG. These explanations fall into four theories each with a variable amount of supporting data. Erectile dysfunction in the 21st century: whom we can treat.T.132:474. (2) there is an increasing pool of affected men given the age demographics in many societies. and following one year of treatment [40]. The open labeled nature of these latter two studies are problematic. This neurotransmitter also acts at presynaptic a2-receptors on the ends of nerve terminals to reduce norepinephrine release. Int J Impot Res 2002. a1-blockers are associated with a low rate of sexual dysfunction.5(2. pathophysiologic and treatment aspects of these two entities. Comparison of mean weighted scores using the DAN-PSS sex score showed improvement of the EF domain by 36% over baseline (2. 5. Conclusions LUTS and sexual dysfunction are highly prevalent in aging men. References [1] McVary KT. 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