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Recently, three new drug principles have been approved for clinical use, the \u03b2<jats:sub>3<\/jats:sub>\u2010adrenoceptor agonist, mirabegron, the phosphodiesterase\u20105 inhibitor, tadalafil and the blocker of afferent and efferent nerves, botulinum toxin. However, new alternatives are continuously being explored. <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> is a filling disorder, and <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> is involved in the generation of afferent impulses. One way of blocking the <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> afferent pathway is through the use of P2X3 receptor antagonists. In animal models, this strategy appears to work very well, but whether it translates effectively to man remains to be established. Evidence suggests that components of the endocannabinoid system are involved in regulation of bladder function. Clinical studies of cannabinoid extracts on <jats:styled-content style=\"fixed-case\">LUTS<\/jats:styled-content> are scarce and essentially restricted to patients with <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>, and the results have so far not been convincing. Amplification of endocannabinoid activity by inhibiting their degradation via fatty acid amide hydrolase inhibitors may be an attractive approach, but no clinical experiences in <jats:styled-content style=\"fixed-case\">OAB<\/jats:styled-content> have been reported. Studies of the lower urinary tract have indicated that several transient receptor potential (<jats:styled-content style=\"fixed-case\">TRP<\/jats:styled-content>) channels, including <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>1, <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>4, <jats:styled-content style=\"fixed-case\">TRPM<\/jats:styled-content>8 and <jats:styled-content style=\"fixed-case\">TRPA<\/jats:styled-content>1, are expressed in the bladder and may act as sensors of stretch and\/or chemical irritation. Animal studies have shown that inhibition of these pathways can be effective for the reduction in bladder activity. However, the roles of these channels for normal function and in pathological states have not been established, and so far adverse effects (hyperthermia) have hampered development of antagonists.<\/jats:p>","DOI":"10.1111\/bcpt.12577","type":"journal-article","created":{"date-parts":[[2016,3,19]],"date-time":"2016-03-19T06:57:18Z","timestamp":1458370638000},"page":"75-85","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["Potential Future Pharmacological Treatment of Bladder Dysfunction"],"prefix":"10.1111","volume":"119","author":[{"given":"Karl\u2010Erik","family":"Andersson","sequence":"first","affiliation":[{"name":"Institute for Regenerative Medicine Wake Forest University School of Medicine Winston Salem NC USA"},{"name":"Aarhus Institute for Advanced Sciences (AIAS) Aarhus University Aarhus 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