An exaggerated exercise pressor reflex (EPR) causes excessive sympatho‐excitation and exercise intolerance in the chronic heart failure (CHF) state. A recent preliminary study from our laboratory suggested that a functional loss of voltage‐gated potassium (Kv) channels in muscle afferent neurons plays a critical role in mediating the exaggerated EPR and afferent sensitization in CHF. However, the molecular mechanisms underlying the Kv channel dysfunction in muscle afferent neurons in CHF remains unclear. Since CHF is associated with chronic inflammation, we investigated the potential effects of chronic inflammation on protein expression of Kv channels in the 50B11 DRG cell line. We used pro‐inflammatory cytokines Interleukin‐6 (IL‐6), Interleukin‐1b (IL‐1β) and tumor necrosis factor alpha (TNFα) to create an inflammatory environment. We investigated the effects of TNFα, IL‐1β and IL‐6 on multiple Kv channel isoforms (Kv1.4, Kv3.4, Kv4.2 and Kv4.3), respectively. Three day exposure of TNFα (10 ng/ml) decreased protein expression of Kv3.4, but increased Kv1.4 protein expression without any change in the protein expression of Kv4.2 and Kv4.3. Similarly, 3‐day exposure of of IL‐1β (10 ng/ml) decreased the protein expression of Kv3.4, but had no effect on protein expression of Kv1.4, Kv4.2 and Kv4.3 in 50B11 cells. Finally, 3‐day exposure of IL‐6 (10 ng/ml) decreased the protein expression of Kv3.4, Kv4.2 and Kv4.3 without any effect on Kv1.4 (Table 1). These data suggest that chronic exposure of inflammatory cytokines cause the reduction of Kv channels in DRG neurons. However, each cytokine may have a slightly different impact on individual Kv channel isoforms.Support or Funding InformationThis work was supported by grants from the National Heart, Lung, and Blood Institute (R01HL121012‐A1 to HJW and in part, by R01HL126796‐A1 to HJW and IHZ).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.