Leaky urothelium and/or vesical ischemia enable urinary potassium to cause idiopathic urgency/frequency syndrome and urge incontinence.

Urine contains up to 10 times more potassium (K+) than blood plasma. Hence, extracellular K+ concentration of the bladder wall can increase secondary to a leaky urothelium (GAG layer deficiency) and/or vesical ischemia (reduced washout) at low filling volumes. Consequent sensory afferentiated excitation/depolarization of the detrusor leads to urgency/frequency and facilitates the onset of 'uninhibited' contractions. This feature, in association with a weak rhabdosphincter, causes urge incontinence. The non-neuromuscular (non-reflexive) origin explains refractoriness to any neurotransmitted inhibition. Even successful interference with contractility (Ca2+) leaves depolarization unaffected. Accordingly, comparative cystometry (saline versus 0.2 M KCl) is recommended in order to comprise better former falsely under-diagnosed 'normals' as well as former undiscovered urge incontinence, and thus indications for bladder neck surgery as well as neuromuscular drug treatment. Future first-line therapy in idiopathic storage disorders should be directed to the GAG layer, vesical blood flow (K+ washout) and the rhabdosphincter.