Differential expression and function of nicotinic acetylcholine receptors in the urinary bladder epithelium of the rat

Key points •  It has been previously shown that stimulation of urothelial nicotinic acetylcholine receptors (nAChRs) can alter reflex bladder activity in the rat; the current study examines this further. •  Stimulation of rat urothelial cells with an α7 nAChR agonist increases intracellular calcium through internal stores and decreases basal ATP release. •  Stimulation with an α3* nAChR agonist increases intracellular calcium through extracellular influx and increases basal ATP release. •  Infusion of an α3* agonist into the bladder lumen of the rat increases reflex bladder activity, which is blocked by intra‐arterial administration of a purinergic antagonist. •  The cellular effects of α3* stimulation are blocked when the cells are pretreated with an α7 agonist, suggesting cross‐talk between the receptors: this cross‐talk may be mediated through protein kinase A or protein kinase C.