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55 nmol kg?1) were administered simultaneously, and 3 min later the ganglionic C59 research buy stimulation was repeated. Role of NO on the pro-erectile facilitator effects of AVE 0991 The role of NO on the effects of AVE 0991 was evaluated using the NOS inhibitor l-NAME. A submaximal stimulus was determined as described previously (da Costa Gon?alves et al. 2007), and applied to the MPG for a duration of 2 min. Ten minutes were allowed for the recovery of normal erectile function of the animals. Subsequently, l-NAME (200 ��g kg?1) was injected intracavernously, and after 10 min the ganglionic stimulation was repeated. After 10 min of recovery, AVE 0991 (1.55 nmol kg?1) or vehicle was infused. Three minutes after the beginning of the infusion, the submaximal stimulus was applied again while the CCP and MAP were continuously recorded. All results are expressed as means �� SEM. Statistical analysis of the effect of AVE 0991 on the ganglionic stimulation-induced increases in CCP/MAP ratio, as well as the intracavernosal effect of A-779, were buy MLN8237 performed by two-way ANOVA followed by Bonferroni post hoc test. To analyse the influence of l-NAME on the effect of AVE 0991, a one-way ANOVA followed by Bonferroni post hoc test was used. A value of P Aldosterone and 155 nmol kg?1) did not change the CCP/MAP ratio induced by electrical stimulation of MPG (Fig. 1A and B). Vehicle administration did not change the CCP/MAP ratio. We also evaluated the role of the Mas receptor on the pro-erectile facilitator effects of AVE 0991. The Mas antagonist A-779 (155 pmol kg?1 min?1) was administered simultaneously with AVE 0991 (1.55 nmol kg?1) into the corpus cavernosum. As shown in Fig. 2, A-779 abolished the potentiation of CCP/MAP increase induced by AVE 0991 on the erectile response (Fig. 2). The involvement of NO release in the effect of AVE 0991 was determined by using the NOS inhibitor l-NAME. Intracavernousal injection of l-NAME (200 ��g kg?1) attenuated the CCP/MAP increase induced by the submaximal electrical stimulation (Fig. 3, top panel), which was not restored by AVE 0991 (Fig. 3, bottom panel). These results indicate that AVE 0991 potentiates the penile erectile response through Mas/NO-mediated mechanisms. In this study, we have obtained clear evidence that AVE 0991 facilitates penile erectile function in rats. This finding extends our previous observations using Ang-(1?7) (da Costa Gon?alves et al. 2007).