The Ameliorating Effect of Exogenous Melatonin on Urinary Bladder Function in Hyperosmolar Bladder Overactivity and its Influence on the Autonomic Nervous System Activity

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.

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Bladder Problems

Dementia with Lewy Body and Parkinson's Disease Patients ◽

10.1093/oso/9780199977567.003.0023 ◽

2013 ◽

Author(s):

J. Eric Ahlskog

Keyword(s):

Nervous System ◽

Autonomic Nervous System ◽

Neurogenic Bladder ◽

Soft Tissues ◽

Bladder Wall ◽

Bladder Function ◽

System Control ◽

Autonomic Nervous ◽

Age Related ◽

The Central Nervous System

Urinary problems occur with normal aging. In women they often relate to the changes in female anatomy due to the delivering of babies. With superimposed age-related changes in soft tissues, laxity may result in incontinence (loss of urinary control), especially with coughing, laughing, or straining. In men the opposite symptom tends to occur: urinary hesitancy (inability to evacuate the bladder). This is due to constriction of the bladder outlet by an enlarging prostate; the prostate normally surrounds the urethra, through which urine passes. DLB and PDD are often associated with additional bladder problems. Recall that the autonomic nervous system regulates bladder function and that this system tends to malfunction in Lewy disorders. Hence, reduced bladder control is frequent among those with DLB, PDD, and Parkinson’s disease. This condition is termed neurogenic bladder, which implies that the autonomic nervous system control of bladder reflexes is not working properly. This may manifest as urgency with incontinence or hesitancy. Neurogenic bladder problems require different strategies than those used for treating the simple age-related problems that develop in mid-life and beyond. Moreover, there are certain caveats to treatment once a neurogenic bladder is recognized. The bladder is simply a reservoir that holds urine. It is located in the lower pelvis and is distant from the kidneys. The kidneys essentially filter the circulating blood and make the urine. The urine flows down from the kidneys into the bladder, as shown in Figure 14.1. Normally, as the bladder slowly fills with urine, a reflex is triggered when it is nearly full. This results in conscious awareness of the need to urinate, plus it primes the reflexive tendency of the bladder to contract in order to expel the urinary contents. The bladder is able to contract because of muscles in the bladder walls. Normally, nerves activate these muscles at the appropriate time, which forcefully squeeze the bladder, expelling the urine. Nerve sensors in the bladder wall are activated by bladder filling and transmit this information to the central nervous system, ramping up bladder wall muscle activity.

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