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Plasma levels of endothelin‐1, angiotensin II, nitric oxide and prostaglandin E 2 in the venous and cavernosal blood of patients with erectile dysfunction
Author(s) -
El Melegy Nagla Taha,
Ali MohamedEsam M.,
Awad Efat M.A.
Publication year - 2005
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2005.05780.x
Subject(s) - venous blood , psychogenic disease , angiotensin ii , medicine , nitric oxide , endothelin receptor , endothelin 1 , endocrinology , renin–angiotensin system , erectile dysfunction , radioimmunoassay , blood pressure , receptor , radiology
OBJECTIVES To determine the alterations in the plasma levels of endothelin‐1, angiotensin II, nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) in the venous and cavernosal blood of patients with organic and psychogenic erectile dysfunction (ED). PATIENTS, SUBJECTS AND METHODS The study included 32 patients complaining of ED; they were subdivided into two equal groups with either organic or psychogenic ED. Fifteen healthy potent age‐matched male volunteers were enrolled as a control group. For each patient, venous and cavernosal blood samples were obtained, while venous blood was obtained from the controls. RESULTS There were significantly greater mean plasma levels of endothelin‐1 and angiotensin II, and significantly lower mean plasma levels of NO and PGE 2 , in the venous blood of patients with ED than in the controls. Patients with organic ED had significantly higher levels of endothelin‐1 and significantly lower levels of NO in both venous and cavernosal blood than had those with psychogenic ED. There were significant positive correlations in both venous and cavernosal blood between endothelin‐1 and angiotensin II, and between NO and PGE 2 in all patients with ED and the two subgroups. There were significant negative correlations between venous and cavernosal endothelin‐1 and NO, endothelin‐1 and PGE 2 , angiotensin II and NO, and between angiotensin II and PGE 2 . CONCLUSION The present results suggest that endothelin‐1 could be a clinical marker of diffuse endothelial disease manifested by ED. As angiotensin‐converting enzyme (ACE) activity controls angiotensin II there might be a rationale for the use of ACE inhibitors to prevent or treat ED. NO and PGE 2 may provide new strategies for the pharmacological treatment of ED.