Prof. Dr.Mohamed Hamdy Abouel-Hassan

nonadrenergic/
noncholinergic
Review of literature
does contribute indirectly to penile erection by (1) presynaptic inhibition of
adrenergic neurons and (2) stimulation of the release of NO from endothelial
cells (Saenz de Tejada et al, 1989a).
Most researchers now agree that NO released from
(NANC) neurotransmission and from the
endothelium is the principal neurotransmitter mediating penile erection. NO
increases the production of cGMP, which in turn relaxes the cavernous
smooth muscle (Holmquist et al, 1991; Kim N et al, 1991; Pickard et al,
1991; Burnett et al, 1992; Knispel et al, 1992; Trigo-Rocha et al, 1993,).
NO and cGMP in Relaxation of Smooth Muscle
NO was first described in 1979 as a potent relaxant of peripheral vascular
smooth muscle, with an action mediated by cGMP (Gruetter et al, 1979).
Subsequently, endothelium-derived relaxing factor was identified as NO or a
chemically unstable nitroso precursor (Ignarro et al, 1987; Palmer et al,
1987). NO is synthesized from endogenous 1
inhibited by N-substituted analogues of 1-arginine, such as N
arginine, N
-nitro-l-arginine,
hemoglobin.
and N
-amino-l-arginine.
-arginine
by NOS, which can be
-methy1-1-
NO is inactivated by
There are three distinct forms of NOS (neuronal [nNOS or NOS-1],
macrophage and other immune cells [iNOS or NOS-2], and endothelial
[eNOS or N
OS-3]
)
.
that increase intracellular C
The NOS-1 and NOS-3 forms are activated by agents
a
2+
concentration, including the vasodilators
acetylcholine and bradykinin. The NOS in immune cells is induced not by
Ca
2
+
but by cytokines. NOS have multiple regulatory sites, including binding
sites for nicotinamide-adenine dinucleotide phosphate (NADPH), flavin
adenine dinucleotide (FAD) and flavin mononucleotide (FMN), and
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