Data issued from morphological and physiological experiments suggests that
the noradrenergic system, through ascending pathways to the brain and desce
nding pathways to the spinal cord, may regulate male sexual functions. Adre
noceptors have been shown to be present in the brain and spinal cord of ani
mals and humans. The activity of spinal preganglionic neurons is modulated
by noradrenaline. Pharmacological approaches aiming at selectively targetin
g alpha(1)- or alpha(2)-adrenoceptors have been conducted in patients with
erectile dysfunction or in monkeys and rats in a variety of tests. Briefly,
conclusions arising from these studies are: activation of alpha(1)-adrenoc
eptors facilitates copulation, where activation of alpha(2)-adrenoceptors i
nhibits copulation. alpha(2)-adrenoceptors antagonists like yohimbine facil
itate sexual behavior, reducing ejaculation latency in male rats and increa
sing their sexual motivation. Furthermore, yohimbine induces copulation in
rats either castrated or sexually naive. In contrast, activation of alpha(1
)-adrenoceptors depresses sexual responses in another context, i.e. reflexi
ve erections. Activation of alpha(2)-adrenoceptors activates reflexive erec
tions in rats, and alpha(2)-adrenoceptors antagonists (yohimbine) inhibit t
hem. Today's challenge is to separate the effects of any drug acting at the
level of the alpha-adrenoceptors on the central vs, peripheral control of
sexual functions, on the brain vs. spinal cord control of the same function
s, and the search for any specialization of alpha-adrenoceptors subtypes in
a given sexual function. Treatment of sexual dysfunctions in man (e.g. eja
culation) focusing on the spinal cord as a pharmacological target should al
so be expanded. Finally, considering the similarities between neural networ
ks controlling male and female sexual functions, the treatment of female se
xual dysfunction with comparable pharmacological approaches should be evalu
ated.