The persistent low-grade mucosal inflammation in the gastrointestinal tract is a main pathophysiological basis of the pathogenesis of post-infectious or inflammatory irritable bowel syndrome (PI-IBS) and visceral hypersensitivity is the core mechanism of PI-IBS. The sensory facilitation caused by the increase of neuronal excitation of spinal afferent nerve pathway plays the most important role in abnormal visceral nociception, but the underlying mechanisms have not been fully understood. Review of recent studies suggests that under the condition of chronic inflammation, the large conductance calcium-activated potassium channel (BKCa) of the cell membrane of neurons of spinal afferent nerve in dorsal root ganglions is vital in the reaction mechanism of visceral hypersensitivity of PI-IBS by changing the excitation of neurons and involving the regulation of gastrointestinal sensitivity.