In this study, we modeled the production, transport and consumption of nitric oxide (NO) in the renal medullary microcirculation under basal conditions. In order to yield agreement with reported NO concentrations of ~ 60 - 140 nM in medullary tissues (67, 68) and 3 nM in plasma (54), the permeabilities of RBCs, vascular walls, and pericytes to NO are all predicted to lie between 0.01 and 0.1 cm/s, and the NO production rate by vasa recta endothelium is estimated to be on the order of 10^-14 µmol/µm²/s. Our results suggest that the concentration of NO in red blood cells (RBCs), which is essentially controlled by the kinetics of NO scavenging by hemoglobin, is about 0.01 nM, that is, 10³ times lower than that in plasma, pericytes and interstitium. Since the basal concentration of NO in pericytes is on the order of 10 nM, it may be too low to active guanylate cyclase, i.e., to induce vasorelaxation. Our simulations also indicate that basal superoxide concentrations may be too low to affect medullary NO levels, but that under pathological conditions superoxide may be a very significant scavenger of NO. We also found that although oxygen is a negligible NO scavenger, medullary hypoxia may significantly enhance NO concentration gradients along the cortico-medullary axis.