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Updated: Feb 20, 2026

Treatment Model for Young Patients with Psychogenic Erectile Dysfunction and Resultant Infertility
Published on: May 30, 2025
Relationship between asymmetric dimethylarginine, nitrite and genetic polymorphisms: Impact on erectile dysfunction
Ana Maria Milanez Azevedo1, Guilhermo Brites-Anselmi2, Lucas Cezar Pinheiro1
1Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Nitrite levels correlate with poorer Sildenafil response in erectile dysfunction patients. Genetic variations in DDAH1 and DDAH2 also impact treatment outcomes, particularly in post-prostatectomy patients.
Area of Science:
- Biochemistry
- Pharmacology
- Urology
Background:
- Sildenafil is a primary treatment for erectile dysfunction (ED), but patient response varies.
- Nitric oxide (NO) signaling is key to Sildenafil's efficacy.
- Asymmetric dimethylarginine (ADMA) inhibits NO production and is metabolized by Dimethylarginine Dimethylaminohydrolase (DDAH) enzymes.
Purpose of the Study:
- To investigate the association between plasma ADMA and nitrite levels with Sildenafil responsiveness in ED patients.
- To explore the relationship between genetic polymorphisms in DDAH1 and DDAH2 genes and Sildenafil treatment outcomes.
Main Methods:
- 140 patients were divided into Clinical Erectile Dysfunction (CED) and Post-Prostatectomy Erectile Dysfunction (PPED) groups.
- Erectile function was assessed using the International Index for Erectile Function Questionnaire before and after Sildenafil treatment.
- Plasma ADMA and nitrite levels were measured, and genetic polymorphisms in DDAH1 and DDAH2 were analyzed.
Main Results:
- Higher nitrite levels were associated with a worse response to Sildenafil (r = -0.25, P = 0.040).
- DDAH1 polymorphisms (rs1554597, rs18582) correlated with altered ADMA levels in the CED group.
- DDAH2 polymorphisms were linked to modified Sildenafil responsiveness in the PPED group (B = +0.19, P = 0.027).
Conclusions:
- Plasma nitrite levels may predict poor Sildenafil response in ED.
- Genetic variations in DDAH enzymes influence Sildenafil efficacy, suggesting potential personalized treatment approaches.
- Further research into ADMA, DDAH, and NO pathways could optimize ED therapy.
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