title: The ameliorating effect of exogenous melatonin on urinary bladder function in hyperosmolar bladder overactivity and its influence on the autonomic nervous system activity.
abstract: This study was designed to investigate the effects of melatonin on the bladder hyperactivity in hyperosmolar-induced overactive bladder (OAB) rats. Additionally, the influence of melatonin on the autonomic nervous system (ANS) using heart rate variability (HRV) analysis was assessed. 40 rats were divided into four groups: I--control (n = 12), II--rats with hyperosmolar OAB (n = 6), III--rats with melatonin pretreatment and hyperosmolar OAB (n = 6) and IV--control with melatonin pretreatment (n = 6). In group III and IV melatonin in dose of 100 mg/kg was given. HRV measurements in 10 rats, as follow: control (n = 2), control after melatonin treatment (n = 2), rats with hyperosmolar OAB without (n = 3), and after (n = 3) melatonin treatment were conducted. This study demonstrates marked influence of melatonin on urinary bladder activity in hyperosmolar-induced OAB rats. These rats showed significantly reduced the detrusor motor overactivity resulting in the improvement of cystometric parameters after melatonin treatment when compared to the control, as follow: a significant increase of intercontraction interval (70%) and functional bladder capacity (67%), as well as a decrease of the basal pressure, detrusor overactivity index and motility index of 96%, 439% and 40%, respectively. ANS activity analysis revealed sympathetic overactivity in OAB rats, and parasympathetic superiority in melatonin treated OAB rats. Melatonin treatment in rats with hyperosmolar OAB (group III) caused significant increase of nuHF parameter (from 51.00 +/- 25.29 to 76.97 +/- 17.43), as well as a decrease of nuLF parameter (from 49.01 +/- 25.26 to 23.03 +/- 17.43) and LF/HF ratio (from 1.280 +/- 0.980 to 0.350 +/- 0.330). In conclusion, melatonin suppresses hyperosmolar OAB, and modulates ANS activity by inhibition of the sympathetic drive. Therefore, melatonin may become a useful agent for OAB management.
authors.affiliation: Department of Pathophysiology, Jagiellonian University, Medical College, Cracow, Poland. kajus13@poczta.onet.pl
authors.forename: Kajetan
authors.initials: K
authors.lastname: Juszczak
authors.forename: Agata
authors.initials: A
authors.lastname: Ziomber
authors.forename: Anna
authors.initials: A
authors.lastname: Machowska
authors.forename: Agata
authors.initials: A
authors.lastname: Furgała
authors.forename: Łukasz
authors.initials: Ł
authors.lastname: Dobrek
authors.forename: Marek
authors.initials: M
authors.lastname: Wyczółkowski
authors.forename: Piotr J
authors.initials: PJ
authors.lastname: Thor
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D008550:Melatonin / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D001743:Urinary Bladder / Q000187:drug effects / Q000503:physiopathology*; D053201:Urinary Bladder, Overactive / Q000503:physiopathology*; D014563:Urodynamics / Q000187:drug effects
chemical_list: D008550:Melatonin