Background Previous studies found that visceral sensitivity is increased in bowel obstruction (BO). We hypothesized that mechanical stress‐induced expression of BDNF in smooth muscle cells (SMC) of the distended bowel plays a critical role in visceral hypersensitivity in BO by altering voltage‐gated K+ channel (Kv) activity in sensory neurons. Methods Partial colon obstruction was maintained in rats for 7 days. Colon‐projecting neurons in the dorsal root ganglia (DRG, T13 to L2) were isolated for electrophysiological and gene expression studies. Key Results Compared to controls, membrane excitability of colon‐projecting DRG neurons was markedly enhanced in BO. The densities of total Kv and transient A‐type (IA) K+ currents, but not sustained delayed IK current, were significantly reduced in the neurons in BO. The mRNA expression of IA subtype Kv1.4 in colon neurons was down‐regulated in BO. Expression of BDNF mRNA and protein was dramatically increased in colonic smooth muscle of the distended segment, but not in the non‐distended aboral segment. Mechanical stretch of colon SMC in vitro increased BDNF expression. Treatment with anti‐BDNF antibody restored total Kv and IA currents of neurons from BO rats. Administration of Trk B inhibitor ANA‐12 blocked BO‐associated changes of neuronal excitability, Kv activity and gene expression in obstruction. Conclusions and Inferences Mechanical stress‐induced expression of BDNF in colon SMC plays a critical role in visceral hypersensitivity in BO by suppressing A‐type K+ currents and gene expression in sensory nerve. These findings help to identify therapeutic targets for distention‐associated abdominal pain in the gut. We found that mechanical stress‐induced expression of BDNF in colon SMC plays a critical role in visceral hypersensitivity in bowel obstruction by suppressing A‐type K+ currents and gene expression in sensory nerve. These findings help to identify therapeutic targets for distention‐associated abdominal pain in the gut.