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Neurogenic bladder dysfunction has many different pathogeneses and one drug or therapeutic mechanism would be unlikely to be effective for all causes. The human prostate and the bladder neck contain a dense population of a1AR and stimulation of those receptors results in increased smooth muscle tone and increased closure of the urethra. In-vitro studies have shown that non-selective β-adrenoreceptor (βAR) agonists like isoprenaline have a pronounced inhibitory effect on the human bladder, causing increases in bladder capacity. Studies have found that symptoms of sensory urgency are associated with increased TRPV1 expression in the trigonal mucosa. An orally active TRPV1 antagonist has shown the ability to completely prevent bladder reflex overactivity triggered by capsaicin infusion. The TRPV4 cation channel has been found to mediate stretch-evoked Ca2+ influx and ATP release in primary urothelial cell cultures, suggesting this is a sensor molecule in detecting bladder distension.
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