The pathophysiology of erectile dysfunction related to endothelial dysfunction and mediators of vascular function.
Standard
The pathophysiology of erectile dysfunction related to endothelial dysfunction and mediators of vascular function. / Maas, Renke; Schwedhelm, Edzard; Albsmeier, Jennifer; Böger, Rainer H.
In: VASC MED, Vol. 7, No. 3, 3, 2002, p. 213-225.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - The pathophysiology of erectile dysfunction related to endothelial dysfunction and mediators of vascular function.
AU - Maas, Renke
AU - Schwedhelm, Edzard
AU - Albsmeier, Jennifer
AU - Böger, Rainer H
PY - 2002
Y1 - 2002
N2 - The incidence of erectile dysfunction increases with diabetes, hypertension, hypercholesterolaemia, cardiovascular disease and renal failure. All these conditions are associated with endothelial dysfunction. This review addresses the pathophysiology of erectile dysfunction with a special focus on new insights into nitric oxide (NO)-mediated pathways, oxidative stress and parallels to endothelial dysfunction. NO appears to be the key mediator promoting endothelium-derived vasodilation and penile erection. The possibility is discussed that elevated plasma concentrations of asymmetrical dimethylarginine (ADMA), an endogenous NO synthase inhibitor, may provide an additional pathomechanism for various forms of erectile dysfunction associated with cardiovascular risk factors and disease. Likewise, the role of endothelium-derived factors mediating NO-independent pathways is evaluated.
AB - The incidence of erectile dysfunction increases with diabetes, hypertension, hypercholesterolaemia, cardiovascular disease and renal failure. All these conditions are associated with endothelial dysfunction. This review addresses the pathophysiology of erectile dysfunction with a special focus on new insights into nitric oxide (NO)-mediated pathways, oxidative stress and parallels to endothelial dysfunction. NO appears to be the key mediator promoting endothelium-derived vasodilation and penile erection. The possibility is discussed that elevated plasma concentrations of asymmetrical dimethylarginine (ADMA), an endogenous NO synthase inhibitor, may provide an additional pathomechanism for various forms of erectile dysfunction associated with cardiovascular risk factors and disease. Likewise, the role of endothelium-derived factors mediating NO-independent pathways is evaluated.
M3 - SCORING: Zeitschriftenaufsatz
VL - 7
SP - 213
EP - 225
JO - VASC MED
JF - VASC MED
SN - 1358-863X
IS - 3
M1 - 3
ER -