Plasma levels of endothelin-1, angiotensin II, nitric oxide and prostaglandin E2 in the venous and cavernosal blood of patients with erectile dysfunction
Article first published online: 13 OCT 2005
Volume 96, Issue 7, pages 1079–1086, November 2005
How to Cite
El Melegy, N. T., Ali, M.-E. M. and Awad, E. M.A. (2005), Plasma levels of endothelin-1, angiotensin II, nitric oxide and prostaglandin E2 in the venous and cavernosal blood of patients with erectile dysfunction. BJU International, 96: 1079–1086. doi: 10.1111/j.1464-410X.2005.05780.x
- Issue published online: 13 OCT 2005
- Article first published online: 13 OCT 2005
- Accepted for publication 24 May 2005
- erectile dysfunction;
- angiotensin II. nitric oxide;
- prostaglandin E2
To determine the alterations in the plasma levels of endothelin-1, angiotensin II, nitric oxide (NO) and prostaglandin E2 (PGE2) 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.
There were significantly greater mean plasma levels of endothelin-1 and angiotensin II, and significantly lower mean plasma levels of NO and PGE2, 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 PGE2 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 PGE2, angiotensin II and NO, and between angiotensin II and PGE2.
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 PGE2 may provide new strategies for the pharmacological treatment of ED.