Detrusor muscle

The detrusor muscle is the smooth muscle component of the urinary bladder wall, serving as the primary effector for both urine storage and voiding [StatPearls: Physiology, Bladder]. While often discussed as a therapeutic target in clinical urology, it is an anatomical tissue rather than a single molecular entity; its function is regulated by a variety of receptors, most notably the muscarinic M3 and beta-3 adrenergic receptors [NIH: PMC2897743]. During the storage phase, the detrusor remains relaxed via sympathetic stimulation of beta-3 receptors, allowing the bladder to expand to accommodate urine [PubMed: 15831051]. Micturition is initiated by parasympathetic signaling, where acetylcholine binds to M3 receptors to induce the coordinated contraction necessary for bladder emptying [NCBI: NBK534811]. Pathological conditions such as overactive bladder (OAB) are characterized by detrusor overactivity, leading to symptoms of urgency, frequency, and urge incontinence [Mayo Clinic: Overactive Bladder]. Pharmacological management involves modulating these pathways using antimuscarinic agents to suppress unwanted contractions or beta-3 agonists to enhance relaxation and storage capacity. In cases of refractory detrusor overactivity, botulinum toxin may be injected directly into the muscle to inhibit acetylcholine release at the neuromuscular junction.

Other names

Detrusor urinae muscleBladder smooth muscleTunica muscularis vesicae urinariaeBladder wall muscle

Pharmacological modulation occurs via antagonism of muscarinic M3 receptors to reduce contractility, agonism of beta-3 adrenergic receptors to facilitate bladder relaxation and storage, and inhibition of acetylcholine release at the neuromuscular junction via botulinum toxin.