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   <subfield code="D">G.</subfield>
   <subfield code="u">Department of Urology, University of Innsbruck, Innsbruck, Austria</subfield>
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   <subfield code="a">Leaky urothelium and/or vesical ischemia enable urinary potassium to cause idiopathic urgency/frequency syndrome and urge incontinence</subfield>
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   <subfield code="a">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 nonneuromuscular (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 underdiagnosed ‘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.</subfield>
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   <subfield code="a">The International Urogynecology Journal, 1996</subfield>
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   <subfield code="a">Idiopathic urgency/frequency</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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