Abstract
Stress urinary incontinence (SUI) is a very common condition that affects an average of 49% (24–75%) of incontinent women between 18 and 90 years of age [1] . SUI incontinence is much less common in men than in women by a 1:2 ratio, ranging from 2 to 39% with advancing age [2] . Although it is not a life-threatening condition, SUI may produce a considerable impact on female quality of life. Treatment of SUI is indicated if it begins to affect the sufferer’s quality of life and if the symptom cannot be properly managed by an increase of voluntary micturition or reduction of physical activity. Possible therapies range from absorbent pads and pelvic floor muscles training (PFMT) to several drugs, devices, and surgical procedures. Various drugs, including estrogens, α -adrenoceptor agonists, β -adrenoceptor agonists, and tricyclic antidepressants have been used off label. With the advent of new targets and drugs with a different mechanism of action, pharmacological treatment of SUI is currently regaining interest. There are several factors involved in the pathogenesis of SUI including the urethral support, the bladder neck function, and the function of the muscles of the urethra and pelvic floor [3] . As women with SUI have lower resting urethral pressures than age-matched continent women [4, 5] , it appears likely that there is a reduced urethral closure pressure in most women with SUI. Consequently, it seems logical to increase urethral pressure in order to improve continence. Urethral closure is the result of several contributing factors, including tone of urethral smooth and striated muscle and passive properties of the vasculature of urethral lamina propria. Although the relative contribution of each of these factors to intraurethral pressure is not fully understood, there is ample pharmacological evidence that a substantial part of urethral tone is mediated through stimulation of a -adrenoceptors in the urethral smooth muscle by release of norepinephrine. Lack of estrogens, mainly in elderly women, may be another contributing factor promoting a lack of mucosal function [6] . Pharmacotherapies for SUI aim to increase intraurethral closure forces by increasing tone in the urethral smooth and striated muscles. Several drugs may contribute to achievement of this goal, but limited efficacy or side effects often have limited their clinical use.
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