Does the clinical efficacy of vardenafil correlate with its effect on the endothelial function of cavernosal arteries? A pilot study

Мазо, Е Б; Гамидов, С. И.; Iremashvili, Vyacheslav V.

doi:10.1111/j.1464-410x.2006.06433.x

Cited by 11 publications

(14 citation statements)

References 24 publications

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“…Additionally, the same therapeutic regimen with tadalafil resulted in an increase in cEPCs mobilization and ameliorated endothelial function, as assessed by FMD [113]. Another report demonstrated a positive correlation between PNORT increase and erection improvement after vardenafil therapy [114]. Accordingly and considering our histological [47] and clinical studies [104], we assume that the response to PDE5I might be correlated to the PNORT.…”

Section: Therapeutic Relevance Of Endothelial Dysfunction In Ed Patientsmentioning

confidence: 55%

The Endothelial–Erectile Dysfunction Connection: An Essential Update

Costa

Virag²

2009

The Journal of Sexual Medicine

109

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Introduction The endothelial monolayer plays a crucial role in the vasodilation and hemodynamic events involved in erection physiology. Due to its relevant functions, a close link has been established between endothelial integrity and erectile dysfunction (ED). Endothelial dysfunction is induced by the detrimental actions of vascular risk factors (VRFs), identified as common correlates for the development of cardiovascular disease and ED. It is currently recognized that ED is the early harbinger of a more generalized vascular systemic disorder, and, therefore, an evaluation of endothelial health in ED patients should be of prime relevance. Several noninvasive methods for endothelial function assessment have been proposed, including the Penile Nitric Oxide Release Test (PNORT). Aim To highlight the most recent gathered knowledge on basic and clinical mechanisms underlying loss of cavernosal endothelial function promoted by VRFs and to discuss local and systemic methods for endothelial function assessment in ED individuals, focusing on the PNORT. Main Outcome Measures A complete revision on the novel basic and clinical links between endothelial and ED. Methods A systematic review of the literature regarding the aforementioned issues. Results Risk factor-associated cavernosal endothelial dysfunction is mostly induced by unifying mechanisms, including oxidative stress and impaired endothelial nitric oxide functional activities, which present clinically as ED. Several techniques to evaluate endothelial dysfunction were revised, with advantages and limitations debated, focusing on our detailed expertise using the PNORT method. Conclusions The established endothelial–erectile dysfunction connection was thoroughly revised, from basic mechanisms to the clinical importance of endothelial dysfunction assessment as diagnosis for generalized vascular disease. Further studies are required to disclose efficient approaches to repair disabled endothelium and both restore and prevent endothelial dysfunction.

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Section: Therapeutic Relevance Of Endothelial Dysfunction In Ed Patientsmentioning

confidence: 55%

The Endothelial–Erectile Dysfunction Connection: An Essential Update

Costa

Virag²

2009

The Journal of Sexual Medicine

109

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“…Recent evidence suggest that men with ED, but no clinical cardiovascular disease have a peripheral vascular defect in endotheliumdependent and endothelium-independent vasodilatation that occurs before the development of other overt functional or structural systemic vascular disease and is independent of other traditional cardiovascular risk factors [50]. When these subjects are investigated for endothelial dysfunction, the capacity to produce nitric oxide is often impaired and results in impaired response to oral PDE5 inhibitors [54,55]. However, despite promising preliminary data, endothelial function tests have not been standardized yet, as a part of diagnostic approach to male ED; therefore, we do emphasize that they should be performed for research purposes only.…”

Section: New Potential Use Of Ultrasound For Detecting Endothelial Dymentioning

confidence: 99%

The Role of Penile Color-Duplex Ultrasound for the Evaluation of Erectile Dysfunction

Aversa

Sarteschi

2007

The Journal of Sexual Medicine

122

105

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Introduction In the era of orally active agents, dynamic penile color-duplex ultrasound (D-PCDU) is not considered a necessary first screening for all patients with erectile dysfunction (ED). Various parameters, such as peak systolic flow velocity, end diastolic velocity, resistance index, acceleration time, and degree of arterial dilatation, have been suggested for the diagnosis of vascular ED by D-PCDU. Aim To highlight the clinical utility and evidence-based interpretation of D-PCDU criteria. Methods Extensive, unsystematic PubMed literature search reviewing relevant data on D-PCDU in the evaluation of male ED. Results The advantage of ultrasound is the minimally invasive nature of the procedure and the ability to screen patients to identify a normal arterial response of cavernous arteries. Men with sexual dysfunctions above 55 years of age and comorbidities are more likely to have multi-organ vascular dysfunction and may necessitate further testing because erectile failure may be the first presenting symptom requiring investigation and treatment even in the absence of cardiovascular risk factors. All patients affected with Peyronie's disease and younger men with persistent ED, a history of pelvic traumas, or fractures of the penile shaft should be offered ultrasonographic penile blood flow studies before referral to surgery or more invasive vascular investigations. Conclusions In the near future, D-PCDU may be used in preference to patients presenting with or without vascular risk factors, particularly those not responding to first-line orally active drugs and seeking an explanation as to why these agents failed.

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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%

“…155,166 In addition, the dosage of a PDE5 inhibitor for achieving effectiveness for clinical symptoms increases in relation to the severity of ED/LUTS/BPH. 155,157,167 These findings suggest that the NO-PDE5-cGMP pathway directly affects the development and maintenance of ED/LUTS/BPH. It is clinically important to confirm the safety and efficacy of PDE5 inhibitors in different subgroups of LUTS/BPH.…”

Section: Pde5 and Vascular Functionmentioning

confidence: 81%

“…Indeed, several investigators have shown that endothelial function, as an index of the NO–PDE5–cGMP pathway, correlated with the severity of ED/LUTS/BPH . In addition, the dosage of a PDE5 inhibitor for achieving effectiveness for clinical symptoms increases in relation to the severity of ED/LUTS/BPH . These findings suggest that the NO–PDE5–cGMP pathway directly affects the development and maintenance of ED/LUTS/BPH.…”

Section: Pde5 and Vascular Functionmentioning

confidence: 98%

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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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Does the clinical efficacy of vardenafil correlate with its effect on the endothelial function of cavernosal arteries? A pilot study

Cited by 11 publications

References 24 publications

The Endothelial–Erectile Dysfunction Connection: An Essential Update

The Endothelial–Erectile Dysfunction Connection: An Essential Update

The Role of Penile Color-Duplex Ultrasound for the Evaluation of Erectile Dysfunction

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

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