The primate model has been used for investigations on the physiology a
nd pharmacology of erection. Recent in vitro investigations indicate t
hat nitric oxide acts as the mediator of penile erection, but in vivo
primate studies are needed to corroborate these findings. Penile erect
ions were induced in a primate model using intracavernosal injections
of nitric oxide donors s-nitrocysteine (NO-CYS) and sodium nitroprussi
de (SNP), and acetylcholine (ACh) which stimulates the formation of ni
tric oxide. Penile length and intracavernosal pressures following agon
ist injection were compared with baseline (flaccid) and control erecti
ons (elicited by injection of a papaverine/phentolamine/PGE(1) standar
d mixture). Dose-response curves for each drug were determined with re
spect to maximal intracavernosal pressure, duration of effect and peni
le length, and systemic arterial pressure was monitored. All three age
nts induced erections, with dose-dependent increases in cavernosal pre
ssure and penile length. The maximal cavernosal pressure attained was
similar for all three agents, but the duration of action was significa
ntly shorter with ACh (p < .05). Injection of L-nitro-arginine-methyl-
ester (L-NAME), a nitric oxide synthase inhibitor, before injection of
the nitric oxide donor shortened the duration of effect but did not a
lter maximal cavernosal pressure or penile length attained. Although s
ystemic hypotension was induced by each agent, digital compression at
the base of the penis at the time of injection prevented such changes.
These results suggest that the primate is a useful model to evaluate
the action of substances that induce or inhibit penile erection. The f
indings provide support for the hypothesis that nitric oxide is a medi
ator of penile erection and that nitric oxide donors may be useful in
the treatment of erectile dysfunction.