Current research has centered around the role of nitric oxide in the stimul
ation of cavernosal vasodilation and erection. However, recent evidence fro
m our lab details the importance of endogenous vasoconstrictor mechanisms i
n maintaining a flaccid penile state, and further demonstrates that the inh
ibition of endogenous vasoconstriction is sufficient to stimulate erection
in a rat model. In this article, we suggest inhibition of endogenous vasoco
nstriction as a potential therapeutic avenue in the treatment of erectile d
ysfunction, We also speculate on potential physiologic mechanisms by which
endogenous vasoconstriction is inhibited in order for arousal-initiated vas
orelaxation, and erection, to occur.