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VOL. 73 (4), 963-985, 2007 PHISIOLOGY OF PENILE VASCULATURE...

which there is endothelial dysfunction and reduced NO bioavai-
lability (2-4), suggests the essential role of the vascular endothelium
in the physiology of penile erection, as well as its importance in the
pathogenesis of ED.

Mechanisms that may be related to the endothelial dysfunction
and to the loss of NO bioavailability during vasculogenic ED include
decreased eNOS expression and activity, dysregulation of eNOS
phosphorylation, increased NO scavenging by reactive O2 species
(ROS), eNOS uncoupling, decreased levels of eNOS cofactors and
substrate and increased interaction with contractile signalling
pathways (63). Decreased erectile responses associated with impaired
endothelium-dependent vasodilation and eNOS expression/activity in
CC have been demonstrated in experimental animal models of
diabetes, hypercholesterolemia and hypertension (63, 82-84).
However, little is known about the impaired function of the penile
vasculature and recent evidence suggests that arterial insufficiency
precedes the structural and functional changes in CC leading to ED.
On the other hand, whereas in CC there is a functional impairment
of the NO-mediated endothelium-dependent responses during
vasculogenic ED (82-84), endothelial abnormalities also include
reduced EDHF-type relaxations in penile small arteries from diabetic
men and from a rat model of renal hypertension (65, 85). These
observations suggest the need to investigate the altered functional
responses associated to cardiovascular risk situations leading to ED
in penile arteries and veins.

ACKNOWLEDGEMENTS

This work was supported by grants nº SAF2006-09191 and
BFU2007-67732 from Ministerio de Educación y Ciencia (España).

REFERENCES

(1) LUE, T.F. (2000) Erectile dysfunction. N. Engl. J. Med. 1802-1813.
(2) SULLIVAN, M.E.; THOMPSON, C.S.; DASHWOOD, M.R.; KHAN, M.A.; JEREMY, J.Y.;

MORGAN, R.J. AND MIKHAILIDIS, D.P. (1999) Nitric oxide and penile erection: is
erectile dysfunction another manifestation of vascular disease? Cardiovasc.
Res. 43: 658-665.

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