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THE ROLE OF ENDOTHELIUM IN ERECTILE DISSATISFACTION
Andrea Garolla and Carlo Foresta
Department of Histology, Microbiology and Medical Biotechnologies,
Centre for Male Gamete Cryopreservation, University of Padua, Italy.
andrea.garolla@unipd.it
Endothelial dysfunction seems to be the first step of the atherosclerotic
process. In the past few years, it has been demonstrated that injured
endothelial monolayer is restored by a premature pool of circulating
progenitor cells (PCs) and a more mature one of circulating endothelial
progenitor cells (EPCs). Patients affected by erectile dysfunction
(ED) have low levels of both PCs and EPCs and a subtle endothelial
alteration has been suggested in these subjects.
Even thought there are increasing evidence that estrogens play a
beneficial role on EPCs and, even if debated, on the cardiovascular
system, less is known about androgens. Despite it is well known
that testosterone has a mandatory role in both central and peripheral
modulation of erection, basics of its action are still not completely
understood. Here we investigate the possible Testosterone action
on the regulation of endothelial function and thus on erection.
We evaluated the levels of circulating PCs and EPCs in 10 ED men
(28.6+3.1 years) due to hypogonadotropic hypogonadism (HH) and in
25 age-matched controls. Furthermore, on patients we evaluated the
effect of a prolonged testosterone (T) replacement therapy (testosterone
gel therapy, 50mg/day for 6 months) on PCs and EPCs concentrations,
immunocytochemistry for androgen receptor (AR) on cultured EPCs
and on erectile function.
At baseline HH patients showed a significant reduction of both PCs
and EPCs with respect to controls. T replacement therapy induced
a significant improvement of erectile performances and an increase
of PCs and EPCs with respect to baseline. Immunocytochemistry on
cultured EPCs showed strong expression of the AR.
In conclusion, hypotestosteronemia is associated with a low number
of circulating PCs and EPCs in young HH subjects that could be the
responsible of a subtle endothelial dysfunction and thus of ED.
Testosterone treatment is able to induce an increase in PCs and
EPCs through a possible direct effect on the bone marrow.
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