Dengue virus (DENV) is transmitted to humans by <i>Aedes</i> sp. mosquitoes. Little is known about the cellular and molecular interactions between the virus and the mosquito. The identification of resistance mechanisms could provide insight for the development of control strategies based on genetic manipulation. <i>Objective:</i> To determine the effect of nitric oxide (NO) donors/inhibitors on DENV replication in <i>Aedes aegypti</i> and <i>Anopheles albimanus</i>. <i>Materials and Methods:</i><i>Ae. aegypti</i> and <i>An. albimanus</i> were fed with a blood suspension supplemented with DENV and donors/inhibitors of NO; DENV replication was assessed by immunofluorescence, RT-PCR and qRT-PCR parallel to NO measurement by means of the Griess reaction. <i>Results:</i> DENV replicates at 3×10⁶ genome copies/day/mosquito in <i>Aedes</i>. In comparison, no evidence of virus genome accumulation was detected when 2 m<i>M</i> sodium nitroprusside, a NO donor, were added to the infected blood meal. DENV did not replicate in <i>Anopheles </i>unless 1 m<i>M</i><i>L</i>-N^G-nitroarginine methyl ester, a NO synthesis inhibitor, was added to the infected blood meal, although the absolute viral load was significantly lower than in <i>Aedes</i>. <i>Conclusions:</i> As in humans, NO participates in the control of the virus load in mosquitoes. However, other mechanisms could also be involved in virus resistance in <i>Anopheles</i>.