As described earlier, the stimulation of alpha1-adrenoceptors by norepinephrine leads to increased bladder outlet resistance. It has been shown that alpha1-adrenoceptors influence lower urinary tract function not only through a direct effect on smooth muscle, but also at the level of the spinal cord ganglia and nerve terminals. In this way, they mediate sympathetic, parasympathetic, and somatic outflows to the bladder, bladder neck, prostate, and external urethral sphincter.[13] Blocking these receptors with such agents as prazosin, doxazosin, and terazosin would therefore lead to reduced bladder outlet resistance and, accordingly, to incontinence.[2] One study found that the use of alpha-blockers increased the risk of urinary incontinence in older African American and white women nearly fivefold.[14] Another study showed that almost half of female subjects taking an alpha-blocker reported urinary incontinence.[15] Phenoxybenzamine, a nonselective, irreversible alpha-adrenoceptor antagonist, has been associated with stress urinary incontinence.[1]
It is useful to note that many antidepressants and antipsychotics exhibit considerable alpha1-adrenoceptor antagonist activity