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

FIGURE 2. Penile vasodilatation and erection. Nitric oxide (NO) is released
from parasympathetic nerve terminals and difusses into adjacent smooth muscle
to activate guanylate cyclse (GC). Increased cGMP levels activate protein kinase G

(PKG) which can either stimulate Ca2+-activated K+ channels (KCa) and reduce
intracellular Ca2+, or phosphorylate myosin light chain phosphatase (MLCP) and

reduce Ca2+ sensitivity. PKG can phosphorylate Rho kinase (RhoK) and thus
reduce its activity. Relaxation induced by neural NO increases blood flow and
shear stress on the endothelial cells thereby increasing Akt phophorylation of
eNOS and NO production, and also releasing prostanoids and endothelium-derived
hyperpolarizing factor (EDHF). Nerve-derived acetylcholine (ACh) can either limit
noradrenaline (NA) release from sympathetic nerves through M2 receptors or
stimulate endothelial M3 receptors to induce NO, EDHF and prostanoids release.
Prostanoids activate IP/EP receptors coupled to adenylate cyclase (AC) and increa-
sed cAMP activate protein kinase A (PKA). COX: Cyclooxygenase; CP450: Cyto-
chrome P 450; EC: Endothelial cell.; NT: Nerve terminal; PDE: Phosphodiesterase;

PGI2: Prostacyclin; PLC: Phospholipase C; SMC: Smooth muscle cell.

ENDOTHELIAL DYSFUNCTION AND ERECTILE
DYSFUNCTION

The high prevalence of ED in patients with cardiovascular
disorders such as aging, hypercholesterolemia and hypertension, in

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