Detrusor

The detrusor is the smooth muscle layer of the urinary bladder wall that contracts to expel urine during micturition. It forms the muscularis propria of the bladder, with fibers arranged in intertwined longitudinal, circular, and oblique orientations that enable coordinated, forceful contraction in multiple directions when emptying is needed.

During filling, the detrusor remains relatively relaxed to accommodate increasing urine volume. Micturition is driven by parasympathetic activation: pelvic nerves release acetylcholine, stimulating muscarinic receptors (primarily M3) to cause detrusor contraction. Sympathetic innervation from the hypogastric nerves promotes detrusor relaxation via beta-adrenergic receptors (notably beta-3) and supports continence through the internal urethral sphincter. Somatic innervation via the pudendal nerve controls the external urethral sphincter, coordinating voluntary delay of voiding.

Clinically, detrusor dysfunction can disrupt bladder emptying. Detrusor overactivity causes urgency, frequency, and urge incontinence, often seen in overactive bladder. Detrusor underactivity or acontractile detrusor leads to poor bladder emptying and urinary retention. Neurogenic bladder conditions, aging, diabetes, and spinal or brain injuries can impair detrusor control. Urodynamic studies assess detrusor pressure during filling and voiding to guide management. Treatments for overactivity include antimuscarinic or anticholinergic agents and beta-3 adrenoceptor agonists (for example, mirabegron); underactivity may be managed with bladder training or intermittent catheterization, with pharmacologic options limited and individualized.