Overactive Bladder Pharmacologic Therapy

Daniel H.Biller and G.Willy Davila

The term overactive bladder (OAB) encompasses a wide range of irritative bladder filling and storage symptoms including the symptoms of urinary frequency, urgency,and urge incontinence, alone or in combination. Overactive bladder represents a health condition of increasing public and medical recognition, and because of the wide variation in reported symptoms of OAB, accurate estimates of prevalence and incidence are difficult to calculate.

The underlying pathophysiology of OAB has not been completely elucidated but is believed to be multifactorial. The voiding process is a complex mechanism that integrates the nervous system, including the brain and spinal cord, with the smooth muscle in the bladder and urethra. These circuits control the two integral functions of the bladder: storage and elimination. Theories concerning the pathogenesis of OAB include abnormal excitability or loss of inhibition at various levels of the peripheral and central nervous system and the bladder smooth muscle. Overac-tive bladder can develop as a result of various neurologic disorders, aging, and intrinsic detrusor abnormalities resulting in detrusor overactivity, urgency, and urge incontinence.

Dysfunction at the receptor level has traditionally received the most attention with the major pharmacologic interventions focusing on the muscarinic receptor behavior. The urinary bladder is a heterogeneous organ possessing the high density of muscarinic receptors. At least five receptor subtypes are based on molecular cloning and four receptor subtypes are based on pharmacology. M1, M2, and M3 receptor subtypes have been identified in the human bladder, noting that M2 receptors predominate, but M3 receptors mediate the cholinergic smooth muscle contraction. M2 receptors may have a role in pathologic states, because it has been postulated that the coactivation of M2 receptors enhances the response to M3 stimulation. The muscarinic receptors are widely distributed throughout the central nervous system, and clearly have a role in OAB whether in regulation of detrusor function or in modulating anticholinergic side effects. The exact mechanism of detrusor function and dysfunction remains undefined, with the most likely explanation incorporating disorders at multiple sites within the nervous system and bladder.1

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