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

FIGURE 1. Penile vasoconstriction and flaccidity. Noradrenaline (NA) released
from sympathetic nerves acts on a1 and a2 postsynaptic receptors to elicit

vasoconstrcition and on a2 presynaptic receptors to down regulate its own release
and that of nitric oxide (NO). Activation of a1 adrenoceptors evokes Ca2+ entry
through voltage.dependent (VOC) and receptor-operated channels (ROC)

regulated by Rho kinase (RhoK), thus activating myosin light chain (MLC) kinase
(MLCK) which phosphorylates MLC. Ca2+ sensitization is also activated

through RhoK, protein kinase C (PKC) and tyrosine kinases (TKs) leading to
phosphorylation of MLC phosphatase (MLCP). Neuropeptide Y (NPY) is coreleased

with NA from sympathetic nerves and acts Y1 and Y2 postsynaptic receptors to
enhance NA contractions and on Y2 receptors to limit NA. Adrenaline (A) can
elicit relaxation through b2 adrenoceptors linked to adenylate cyclase (AC), increa-
se of cAMP and activation of protein kinase A (PKA) to enhance K+ efflux and
decrease intracellular Ca2+ and contraction. AII: angiotensin II; NT: Nerve termi-

nal; SMC: Smooth muscle cell.

Non-adrenergic Non-cholinergic (NANC) NO-containing nerves

Penile erection is initiated by activation of parasympathetic
nerves leading to vasodilatation of cavernous and helicine arteries
and to the relaxation of trabecular smooth muscle. However, classical
physiological studies carried out in several animal species and man
showed that erection induced by activation of pelvic or cavernous
nerves was atropine-resistant (5). The neurotransmitter involved in
the erectile responses was further shown to be NO, and it is now
well established that NO locally released from nerves and

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