The intrinsic lymphatic pump is critical to proper lymph transport and is impaired in models of the metabolic syndrome (MetSyn). Lymphatic contractile inhibition under inflammatory conditions has been linked with elevated nitric oxide (NO) production by activated myeloid–derived cells. We utilized a high fructose-fed rat model of MetSyn to test our hypothesis that inhibition of the MLV pump function in MetSyn animals was dependent on NO and was associated with altered macrophage recruitment and polarization within the mesenteric lymphatic vessels (MLV). MetSyn resulted in a greater accumulation of M1-skewed (CD163+MHCII+) macrophages that were observed both within the perivascular adipose tissue and invested along the lymphatic vessels in MetSyn rats when compared to control rats. LECs and LMCs basally express the macrophage maturation polarization cytokines monocyte colony-stimulating factor and dramatically up regulate the M1 promoting cytokine granulocyte/monocyte colony-stimulating factor in response to lipopolysaccharide stimulation. MetSyn MLVs exhibited altered phasic contraction frequency. Incubation of MetSyn MLVs with LNAME or glibenclamide had a partial restoration of lymphatic contraction frequency. The data presented here provide the first evidence for a correlation between alterations in macrophage status and lymphatic dysfunction that is partially mediated by NO and KATP channel in MetSyn rats.