The non-selective dopaminergic agonist apomorphine ( Ki of 101, 32, 26, 2.6, and 10 nM for D1, D2, D3, D4, and D5, respectively) is pro-erectile in the rat and it is thought that the paraventricular nucleus (PVN) mediates these effects (Melis et al, 1987, Succu et al, 2006). The complex neural circuitries which underlie dopamine-induced penile erection remain to be elucidated. However, one potential pathway may involve spinally-projecting oxytocin neurones in the PVN. These neurones may activate the proerectile parasympathetic preganglionic neurones that innervate the penis by releasing oxytocin at the lumbosacral level of the spinal cord. To test this hypothesis, both intracavernous pressure (ICP, via a 25-gauge needle inserted into one corpus cavernosum) and blood pressure (BP, via the femoral artery) were recorded and analysed in urethane-anaesthetised male rats. Erectile responses were dose-dependently (0.01, 0.05, 0.15, 0.25, 1, 5 mg/kg) increased by apomorphine delivered iv through the femoral vein, which also induced transient decreases in blood pressure. The sub-maximal dose of 0.25 mg/kg was selected for use thereafter. An intrathecal injection (directly into the spinal cord at the L4-L6 segmental region) of either vehicle (3 μl isotonic saline) or the oxytocin receptor antagonist, UK-482743-01 (36, 180, 900 ng, n=6-7 per group) was given 5 min prior to apomorphine injection. Both 180 ng and 900 ng of UK-482743-01 effectively inhibited the mean number of erectile responses, but this effect was only statistically significant for the 180 ng injection (p<0.05). The ability of an oxytocin antagonist delivered locally at the level of the sacral parasympathetic nucleus to decrease the erectile activity induced by systemic apomorphine supports the hypothesis that oxytocin release at the lumbosacral spinal cord has a modulatory role in apomorphine-induced penile erection.