Increased cyclic guanosine monophosphate production and endothelial nitric oxide synthase level in mononuclear cells from sildenafil citrate-treated patients with erectile dysfunction

García-Cardoso, J.V.; Vela, Rolando Neri; Mahillo, E; Mateos-Cáceres, Petra J.; Modrego, Javier; Macaya, Carlos; López‐Farré, Antonio

doi:10.1038/ijir.2009.51

Cited by 23 publications

(18 citation statements)

References 49 publications

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“…Whereas available studies, including this one, documented a reduced level of ET-1 in ED patients treated with PDE5i,151734 conflicting results were obtained when biochemical measures of endothelial activation/damage other than ET-1 were considered. The levels of sE-selectin,1718 sPlatelet (P)-selectin and s-Intercellular adhesion molecule-1 (ICAM-1) were not altered in the ED men with VRFs treated with PDE5i;1836 whereas, the same treatment was associated with reduced levels of sICAM,19 sP-selectin and sVascular cell adhesion molecule-1 (VCAM-1) 1837. A limitation in these trials is the lack of a healthy group to determine whether the levels of CAMs released by the endothelial cells were elevated in ED men.…”

Section: Discussionmentioning

confidence: 97%

“…As a secondary outcome, we explored the effect of tadalafil treatment on the circulating markers of endothelial cell damage/dysfunction. The aim of the study was to explore the potential effects of PDE5 inhibition on the laboratory surrogates of endothelial cell damage and repair ability to lend support to the hypothesis of a beneficial effect of this inhibition on vascular homeostasis 111516171819…”

Section: Introductionmentioning

confidence: 99%

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Tadalafil treatment had a modest effect on endothelial cell damage and repair ability markers in men with erectile dysfunction and vascular risk

et al. 2014

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The number of the circulating angiogenic cells (CACs) and colony forming units (CFUs) derived from cultured circulating mononuclear cells (MNCs) represents a laboratory surrogate for endothelial cell repair ability. The serum of men with erectile dysfunction (ED) and vascular risk factors (VRFs) showed an increased level of endothelial cell damage/dysfunction markers and reduced the numbers of CACs and CFUs derived from the cells of healthy men. We analyzed whether treating men with ED and VRFs with the selective phosphodiesterase type 5 inhibitor tadalafil improved the endothelial cell repair ability and reduced the levels of the serum markers of endothelial cell damage/dysfunction. MNCs from healthy men were cultured with 20% serum from 36 ED patients to obtain CACs and CFUs. The ED patients were evaluated before and after 4 weeks of treatment with tadalafil (20 mg every other day) or with a placebo. The tadalafil treatment improved erectile function (P = 0.0028), but had no effect on the inhibitory effects of serum from ED patients on the CACs and CFUs derived from healthy men. The levels of endothelin-1 (P = 0.011) and tissue type plasminogen activator (P = 0.005) were reduced after treatment compared to baseline and those of the placebo group, whereas no changes were observed in the E-selectin levels. The tadalafil treatment in the ED patients with VRFs resulted in only a modest effect on the laboratory measures of the endothelial cell damage/dysfunction and repair ability. The proposed beneficial effect of phosphodiesterase type 5 inhibition on vascular homeostasis requires further analysis.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Tadalafil treatment had a modest effect on endothelial cell damage and repair ability markers in men with erectile dysfunction and vascular risk

et al. 2014

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“…We have also shown that administration of sildenafil induces vasodilation in forearm circulation, and increases both the ACh‐induced and SNP‐induced vasodilation in both smokers and non‐smokers; that sildenafil increases the ratio of ACh‐induced vasodilation to the ratio of SNP‐induced vasodilation; and that the NOS inhibitor l ‐NMMA diminishes the augmentation of ACh‐induced vasodilation after administration of sildenafil, suggesting that inhibition of PDE5 increases NO‐induced vasodilation . The effects of PDE5 inhibitors on endothelial function in patients with ED/LUTS/BPH are summarized in Table . These findings suggest that the mechanism by which PDE5 inhibitors augment or improve vascular function, including endothelial function and vascular smooth muscle function, is mainly activation of the eNOS–NO–cGMP pathway.…”

Section: Pde5 and Vascular Functionmentioning

confidence: 75%

Lower urinary tract symptoms/benign prostatic hypertrophy and vascular function: Role of the nitric oxide–phosphodiesterase type 5–cyclic guanosine 3′,5′‐monophosphate pathway

Higashi

2017

Int J of Urology

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It is well known that there is an association of lower urinary tract symptoms/ benign prostatic hypertrophy with cardiovascular disease, suggesting that lower urinary tract symptoms/benign prostatic hypertrophy is a risk factor for cardiovascular events. Vascular function, including endothelial function and vascular smooth muscle function, is involved in the pathogenesis, maintenance and development of atherosclerosis, leading to cardiovascular events. Vascular dysfunction per se should also contribute to lower urinary tract symptoms/benign prostatic hypertrophy. Both lower urinary tract symptoms/benign prostatic hypertrophy and vascular dysfunction have cardiovascular risk factors, such as hypertension, dyslipidemia, diabetes mellitus, aging, obesity and smoking. Inactivation of the phosphodiesterase type 5-cyclic guanosine 3 0 ,5 0 -monophosphate-nitric oxide pathway causes lower urinary tract symptoms/benign prostatic hypertrophy through an enhancement of sympathetic nervous activity, endothelial dysfunction, increase in Rho-associated kinase activity and vasoconstriction, and decrease in blood flow of pelvic viscera. Both endogenous nitric oxide and exogenous nitric oxide act as vasodilators on vascular smooth muscle cells through an increase in the content of cyclic guanosine 3 0 ,5 0 -monophosphate, which is inactivated by phosphodiesterase type 5. In a clinical setting, phosphodiesterase type 5 inhibitors are widely used in patients with lower urinary tract symptoms/benign prostatic hypertrophy. Phosphodiesterase type 5 inhibitors might have beneficial effects on vascular function through not only inhibition of cyclic guanosine 3 0 ,5 0 -monophosphate degradation, but also increases in testosterone levels and nitric oxide bioavailability, increase in the number and improvement of the function of endothelial progenitor cells, and decrease in insulin resistance. In the present review, the relationships between lower urinary tract symptoms/benign prostatic hypertrophy, the phosphodiesterase type 5-nitric oxidecyclic guanosine 3 0 ,5 0 -monophosphate pathway, vascular function and cardiovascular outcomes are examined.Key words: benign prostatic hypertrophy, lower urinary tract symptoms, nitric oxide, phosphodiesterase type 5-cyclic guanosine 3 0 ,5 0 -monophosphate, vascular function.

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“…Penile rehabilitation programs using PDE5 inhibitors are common practice and have been used extensively in men who underwent a clear bilateral nerve‐sparing RP [21,22]. Briganti et al.…”

Section: Penile Deformities (Penile Length Loss and Curvature) And Edmentioning

confidence: 99%

“…Penile rehabilitation programs using PDE5 inhibitors are common practice and have been used extensively in men who underwent a clear bilateral nerve-sparing RP [21,22]. Briganti et al [15] reported that patients treated with PDE5 inhibitors had significantly higher 3-year erectile function recovery rate compared with patients who did not use any postoperative PDE5 inhibitors (73% vs. 37%, P < 0.001).…”

Section: Penile Deformities (Penile Length Loss and Curvature) And Edmentioning

confidence: 99%

Sexual Rehabilitation and Cancer Survivorship: A State of Art Review of Current Literature and Management Strategies in Male Sexual Dysfunction Among Prostate Cancer Survivors

Chung

Brock

2013

The Journal of Sexual Medicine

100

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Introduction The challenges for prostate cancer survivors include the surveillance of prostate cancer recurrence and management of physical, cognitive, sexual, and socioeconomic quality of life issues. Sexual function remains an important issue in men, who often continue to be interested in sex after prostate cancer treatment. The various post-prostate cancer treatment-related sexual dysfunctions are penile deformities and erectile dysfunction (ED); sexual desire and mental health; ejaculatory and orgasmic dysfunctions; and changes in partner relationship and dynamics. Aims The aim of this study is to provide state of art review of the various male sexual dysfunctions in prostate cancer survivors and the management strategies in sexual rehabilitation. Methods and Materials A literature search for English language original and review articles either published or e-published was performed using PubMed database. Keywords included prostate cancer, prostate cancer treatment, prostate prostatectomy (RP), sexual dysfunction, erectile dysfunction (ED), sexual desire, mental health, ejaculation, orgasmic, climacturia, and relationship. Results There has been considerable volume of publication in recent years on prostate cancer-related male sexual dysfunction. Penile deformities and ED shared similar pathophysiology and that penile smooth muscle fibrosis ultimately results in structural alterations and end-organ failure. Penile rehabilitation using oral phosphodiesterase type 5 (PDE5) inhibitors is considered the standard of care especially in patients who received nerve-sparing RP and should be instituted as soon as possible to protect and prevent corporal endothelial and smooth muscle damage. However, there is no consensus on the exact timing, dose, and duration of PDE5 inhibitors and its impact in non-nerve-sparing RP and other forms of prostate cancer treatment modalities. Current literature on hypoactive sexual desire, ejaculatory, and orgasmic dysfunctions in patients who received prostate cancer treatment is limited. Psychological and sexual counseling play an important role in rehabilitation and treatment of various forms of male sexual dysfunctions. Conclusion While several preventive and treatment strategies for the preservation and recovery of sexual function are available, no specific recommendation or consensus guidelines exist regarding the optimal rehabilitation or treatment protocol. While medical and surgical therapies are effective in erectile function recovery and/or preservation, psychological and sexual counseling are equally important in sexual rehabilitation.

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Increased cyclic guanosine monophosphate production and endothelial nitric oxide synthase level in mononuclear cells from sildenafil citrate-treated patients with erectile dysfunction

Cited by 23 publications

References 49 publications

Tadalafil treatment had a modest effect on endothelial cell damage and repair ability markers in men with erectile dysfunction and vascular risk

Tadalafil treatment had a modest effect on endothelial cell damage and repair ability markers in men with erectile dysfunction and vascular risk

Lower urinary tract symptoms/benign prostatic hypertrophy and vascular function: Role of the nitric oxide–phosphodiesterase type 5–cyclic guanosine 3′,5′‐monophosphate pathway

Sexual Rehabilitation and Cancer Survivorship: A State of Art Review of Current Literature and Management Strategies in Male Sexual Dysfunction Among Prostate Cancer Survivors

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