Recent evidence indicates that endothelin-1 (ET-1) might be a principal vas
oconstrictor in the penis. We report that ET-1 injection into the cavernous
sinuses before erection sharply reduced the magnitude of subsequent erecti
ons. Corpus cavernosum pressure-to-mean arterial pressure ratios (CCP/MAP),
with maximal ganglionic stimulation, were 0.62 +/- 0.05 before ET-1 inject
ion and 0.31 +/- 0.05 after, indicating that ET-1 acted as a vasoconstricto
r. When ET-1 was injected during a maximal neurally induced erection, the a
bility of ET-1 to attenuate subsequent erections was diminished (CCP/MAP 0.
75 +/- 0.02 before ET-1, 0.61 +/- 0.03 after). At submaximal stimulation vo
ltages, injection of ET-1 during erection also attenuated its vasoconstrict
ive effect. Similarly, when ET-1 was injected during erection induced by in
tracavernosal injection of the nitric oxide (NO) donor NOR-1, subsequent er
ections were not significantly suppressed (CCP/MAP 0.53 +/- 0.04 before ET-
1, 0.45 +/- 0.04 after). These findings that ET-1-induced vasoconstriction
is attenuated during erection are consistent with the hypothesis that NO me
diates erection both by initiating pathways that cause smooth muscle relaxa
tion and by inhibiting the vasoconstrictive actions of ET-1.