Testosterone Regulates PDE5 Expression and in vivo Responsiveness to Tadalafil in Rat Corpus Cavernosum

Zhang, Xinhua; Morelli, Annamaria; Luconi, Michaela; Vignozzi, Linda; Filippi, Sandra; Marini, Mirca; Vannelli, Gabriella Barbara; Mancina, Rosa; Forti, Gianni; Maggi, Mario

doi:10.1016/j.eururo.2004.10.021

Cited by 173 publications

(240 citation statements)

References 25 publications

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“…41 Testosterone is a key central and peripheral modulator of erectile function in animal studies. [42][43][44][45] Consistent with these observations, a single-center study of 1050 men seeking new consultation for sexual dysfunction found that 36% had hypogonadism. 46 Buvat and Bou Jaoude, 47 in a compilation of data from 7000 men with ED in 9 large series, reported serum testosterone levels less than 300 ng/dL (to convert to nmol/L, multiply by 0.0347) in 12%, including 4% before and 15% after age 50 years.…”

Section: Recommended Assessments and Risk Clarificationmentioning

confidence: 66%

The Princeton III Consensus Recommendations for the Management of Erectile Dysfunction and Cardiovascular Disease

Nehra

Jackson

Miner

et al. 2012

Mayo Clinic Proceedings

406

338

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The Princeton Consensus (Expert Panel) Conference is a multispecialty collaborative tradition dedicated to optimizing sexual function and preserving cardiovascular health. The third Princeton Consensus met November 8 to 10, 2010, and had 2 primary objectives. The first objective focused on the evaluation and management of cardiovascular risk in men with erectile dysfunction (ED) and no known cardiovascular disease (CVD), with particular emphasis on identification of men with ED who may require additional cardiologic work-up. The second objective focused on reevaluation and modification of previous recommendations for evaluation of cardiac risk associated with sexual activity in men with known CVD. The Panel's recommendations build on those developed during the first and second Princeton Consensus Conferences, first emphasizing the use of exercise ability and stress testing to ensure that each man's cardiovascular health is consistent with the physical demands of sexual activity before prescribing treatment for ED, and second highlighting the link between ED and CVD, which may be asymptomatic and may benefit from cardiovascular risk reduction. T he Princeton Consensus Conference is a multispecialty collaborative tradition dedicated to optimizing sexual function and preserving cardiovascular health. The first conference convened in June 1999 to develop recommendations for clinical management of sexual dysfunction in men and women with known cardiovascular disease (CVD). This conference also provided a multidisciplinary forum for evaluation of the potential cardiovascular risk posed by sexual activity in atrisk patients. The first Princeton Consensus Conference recommendations 1 included stratification of patients by level of cardiac risk associated with sexual activity based on existing CVD. Those at low risk could initiate or resume sexual activity and be treated for sexual dysfunction. For those at high risk, sexual activity was deferred until the cardiac condition was stabilized. The second Princeton Consensus Conference convened in June 2004 and expanded the recommendations of the first conference to emphasize risk factor evaluation and lifestyle management for all men with erectile dysfunction (ED). 2 The second conference recommendations also incorporated new information on the appropriate use of phosphodiesterase type 5 (PDE5) inhibitors in men with ED and concomitant CVD.The third Princeton Consensus Conference took place November 8 to 10, 2010, in Miami Beach, Florida. The group revisited and updated their 2005 recommendations regarding the cardiovascular risk associated with sexual activity in men with known CVD. 2 In addition, the third conference focused on the predictive value of vasculogenic ED in assigning cardiovascular risk in men of all ages, with the primary objective being development of an approach to cardiovascular risk assessment in younger men with ED and no known CVD. The role of testosterone in erectile function and cardiovascular health and the utility of testosterone replacement...

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Section: Recommended Assessments and Risk Clarificationmentioning

confidence: 66%

The Princeton III Consensus Recommendations for the Management of Erectile Dysfunction and Cardiovascular Disease

Nehra

Jackson

Miner

et al. 2012

Mayo Clinic Proceedings

406

338

View full text Add to dashboard Cite

show abstract

“…The expression of 18S rRNA subunit, chosen as reference gene, was quantified with a predeveloped assay (Applied Biosystems) and used for normalization and relative quantitation of the target gene. Data analysis was based on the comparative threshold cycle (C t ) method according to the manufacturer's instructions (Applied Biosystems), as previously described (Zhang et al 2005).…”

Section: Rna Extraction and Quantitative Rt-pcr Analysismentioning

confidence: 99%

Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells

Vignozzi

Cellai²,

Santi³

et al. 2012

Journal of Endocrinology

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121

107

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Progression of benign prostatic hyperplasia (BPH) involves chronic inflammation and immune dysregulation. Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor a, lipopolysaccharide, or CD4 C T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4 C T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon g inducible protein 10, IP10), and Th2 (IL9)-and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-kB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by testosterone cells, an increase in IL10, and a significant reduction of testosterone cells proliferation suggested that DHT exerted a broad antiinflammatory effect on testosterone cells. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses.

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“…[23][24][25][26][27][28] The expression and activity of phosphodiesterase type 5 were shown to be under the control of androgens as well. [29][30][31] This enzyme hydrolyzes cGMP in vascular and trabecular smooth muscle into GMP, leading to smooth muscle relaxation and thus penile flaccidity. In some studies performed in rats and rabbits, this enzyme was shown to be reduced by castration but restored by androgen supplementation.…”

Section: Peripheral Action Of Adt On Male Sexual Behaviormentioning

confidence: 99%

“…In some studies performed in rats and rabbits, this enzyme was shown to be reduced by castration but restored by androgen supplementation. [29][30][31] Thirdly, androgens indirectly maintain endothelial function through the prevention of fibrosis. During erection, smooth muscle expands in a three-dimensional fashion under NO control, and induces the compression of the subtunical venules located externally between the tunica albuginea and the corporal smooth muscle.…”

Section: Peripheral Action Of Adt On Male Sexual Behaviormentioning

confidence: 99%

Impact of androgen deprivation therapy on sexual function

Mazzola

Mulhall²

2012

Asian J Androl

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Many patients with prostate cancer for whom androgen deprivation therapy (ADT) is indicated are young and desire to remain sexually active. In such patients, the side effects of androgen therapy on sexual function can be a source of serious reduction in overall quality of life. Providing the appropriate treatment options in this patient population is therefore essential. Nevertheless, treating such patients is challenging and an understanding of the underlying mechanisms of sexual physiology and pathophysiology is crucial to optimal patient care. In this paper, we reviewed what was known regarding the effects of ADT on sexual function in animal models and we also provided a detailed review on the effects of ADT on sexual health in humans and its treatment.

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Testosterone Regulates PDE5 Expression and in vivo Responsiveness to Tadalafil in Rat Corpus Cavernosum

Cited by 173 publications

References 25 publications

The Princeton III Consensus Recommendations for the Management of Erectile Dysfunction and Cardiovascular Disease

The Princeton III Consensus Recommendations for the Management of Erectile Dysfunction and Cardiovascular Disease

Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells

Impact of androgen deprivation therapy on sexual function

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