Penile erection is a complex physiological process in which the regulation
of penile hemodynamics depends on signal input from central and peripheral
nervous systems, and on the balance and interplay between several local phy
siological mediators (neurotransmitters, vasoactive agents and endocrine fa
ctors), A role for the sympathetic nervous system in attaining or maintaini
ng penile flaccidity and detumescence is well recognized. However, the exac
t mechanisms of alpha-adrenergic receptor mediated erectile function remain
poorly defined, The objective of this review is to summarize data presente
d in the literature and from our laboratory on alpha adrenergic receptors,
and to discuss the conceptual framework by which the alpha-adrenergic recep
tor pathway modulates penile corpus cavernosum smooth muscle contractility,
We will integrate the current state of knowledge of penile erection into o
ne framework encompassing the biochemical and physiological pathways respon
sible for trabecular smooth muscle relaxation (erection) and contraction (d
etumescence), We will focus our discussion on local control mechanisms of a
lpha-adrenergic receptors and explore the following topics: (1) functional
activity of alpha-1 and alpha-2 adrenergic receptors in the physiology of h
uman penile erection; (2) identification, classification and characterizati
on of alpha-1 and alpha-2 adrenergic receptor subtypes in human penile erec
tile tissue; (3) molecular mechanism of action of alpha-1 and alpha-2 adren
ergic receptors in human penile erectile tissue; (4) blockade of alpha-1 an
d alpha-2 adrenergic receptor action by selective and non-selective alpha-l
and alpha-2 adrenergic receptor antagonists (blockers); (5) physiologic (f
unctional) antagonism of alpha-1 and alpha-2 adrenergic receptor activity b
y vasodilators mediating smooth muscle relaxation; and (6) key areas of con
sensus, as well as critical gaps in the existing scientific knowledge conce
rning the rationale and the potential use of alpha-blockers in erectile fun
ction.