A mathematical model was used to investigate the role of the vasodilator nitric oxide (NO) in the regulation of renal afferent arteriole (AA) segmental resistance (SR) following vascular injury. The AA was modeled as a two-dimensional elastic-contractile boundary immersed in a fluid domain. The immersed boundary method was used to quantify the interaction between the fluid and the model AA walls. The model includes a representation of the AA's myogenic response; the convection, diffusion, and degradation of NO; and the relaxation of the model AA walls in response to NO concentration. A focal constriction that reduced flow by ca. 20% was used to simulate vascular injury. In the absence of NO, this focal constriction increased SR, indicating that the myogenic response alone is insufficient to return downstream resistance to its preconstricted value. However, the inclusion of NO released from the injury site, as indicated in the experimental literature, caused sufficient dilation downstream to return SR to its preconstricted value. These simulations suggest that even though NO decays rapidly, it may have important non-local effects. The model provides a new tool for investigating the quantitative contributions of microvascular regulatory mechanisms.