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DOLORES PRIETO Y ALBINO GARCÍA SACRISTÁN ANAL. REAL ACAD. NAC. FARM.

cholinergic neurotransmitter acetylcholine (ACh) relaxes CC smooth
muscle and penile arteries and veins (5, 22, 24, 52), despite the fact
that erection is atropine-resistant. ACh released from cholinergic
nerves during erection probably has a role decreasing sympathetic
adrenergic tone, though its action on prejunctional muscarinic
receptors at sympathetic nerve terminals as reported in other small
arteries and CC (7, 8, 53).

There is a rich presence of peptidergic nerves containing
Vaoactive Intestinal Peptide (VIP) in the penis and nNOS, VIP and
VAChT are co-localized in the same perivascular nerve terminals
around penile arteries and in trabecular smooth muscle (44, 45). VIP
induces potent relaxations in penile arteries and veins (5, 54).
However, VIP antagonists do not inhibit neurogenic relaxations in
penile small arteries but VIP relaxant responses are partially blocked
by NOS inihibition, which suggests that VIP may have a presynaptic
facilitatory role in the nitregic neurotranmission (54).

The synthesis and release of NO in the penile vasculature is
modulated by several factors such as neurotransmitters, hormones,
autacoids and O2 tension. Noradrenaline from sympathetic nerves
down-regulates NO release through a2-adrenoceptors in penile
resistance arteries (55). The expression and activity of NOS can also
be regulated by protaglandins and PGE1 exerts a long term up-
regulation of NO synthesis by increasing the penile content of both
nNOS and eNOS after repeat treatment (56).

Partial O2 pressure (pO2) in the blood of the CC plays a key role
in the regulation of penile haemodynamics. pO2 values are similar to
those of venous blood during flaccidity and they rise to 90-100 mm
Hg during erection, as a result of the increased arerial inflow to the
sinuses (57). Since molecular O2 is a substrate for NO synthesis,
pO2 regulates the ability of CC smooth muscle to relax in response
to EFS of the nerves and endothelium-dependent vasodilators
such as ACh, these NO-dependent responses being progressively
inhibited as a function decreasing pO2 levels (57). Furthermore, both
nNOS and eNOS proteins dramatically decrease in the erectile tissue
during chronic cavernosal isquemia which suggests that arterial
insufficiency and subsequent exposure of erectile tissue to hypoxia
impairs NOS expression and thus NO synthesis and relaxation (58).

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