Peter Zvara, Katarína Zvarová
The overactive bladder is a serious medical problem. Despite significant research efforts to date, its exact etiology is unknown and universally effective treatment is not yet available. Since acetylcholine is the primary excitatory neurotransmitter involved in urinary bladder smooth muscle contraction, anticholinergic agents are the primary compounds used clinically in patients suffering from irritative bladder symptoms. Their effect is based on suppression of muscarinic receptors in the bladder wall and the resultant suppression of the motor function of the detrusor muscle. Patients frequently discontinue treatment with antimuscarinics because of low efficacy and/or significant side effects. The results of research in the past two decades suggest that abnormalities in the sensory innervation of the lower urinary tract play a significant role in the development of bladder overactivity. Vanilloid sensory nerve receptors can be blocked by capsaicin and resiniferatoxin, drugs that have been shown to also reduce detrusor overactivity and suppress irritative voiding symptoms in patients with bladder overactivity. Their use has not been widely accepted due to their high cost, significant side effects and technical problems associated with their administration. Their clear suppressive effect on the non-voiding bladder contractions, however, confirms that sensory nerves play an important role in the etiology of bladder overactivity. In the last 2 decades botulinum toxin A (BTX-A) has been used for treating striated muscle spasticity. BTX-A injected into the wall of the urinary bladder reduces both overactivity and discomfort. This compound is currently studied in both clinical and basic research studies. Therapeutic effect of this compound is probably based on its effect on both the sensory and motor limbs of the micturition reflex. New insights into the pathophysiology of the lower urinary tract have identified new pharmacological targets. Modulation of the sensory nerve function shows great promise, since drugs acting at the level of sensory nerves could reduce irritative symptoms, while preserving detrusor contractility.