Prazosin: a neglected cause of genuine stress incontinence

Prazosin, a common antihypertensive drug, lowers peripheral vascular resistance by selectively blocking alpha-1 adrenergic receptors on arteriolar smooth muscle. Alpha-1 adrenoceptor inhibition also has a relaxant effect on smooth muscle present in the urethra. Between 1985-1990, 58 of 1335 women (4.3%) seen in our urodynamic clinic with urinary incontinence and other urinary symptoms were taking prazosin. The incidence of genuine stress incontinence was significantly higher in women taking prazosin (86.2%) than in the non-prazosin group (65.7%) (P less than .01). Twenty-five of the 45 women contacted had their urinary incontinence improved or cured by prazosin withdrawal. All of these 25 women with prazosin-related urinary incontinence had stress incontinence. The incidence of previous bladder neck surgery in this group was over 50%, with 11 previous vaginal repairs, one Burch colposuspension, and one Aldridge sling procedure. Seven women who were continent after prazosin withdrawal had their urodynamic studies repeated. There was a significant increase in functional urethral length, maximum urethral closure pressure, and abdominal pressure transmission to the urethra following prazosin withdrawal, although no significant change was found in other cystometric measurements including peak flow rate and residual urine volume. In this study, prazosin was a frequently unrecognized cause of stress incontinence in women, many of whom had unsuccessful and possibly unnecessary surgery.