Bladder detrusor smooth muscle hyperreactivity (DO)

Bladder detrusor smooth muscle hyperreactivity, clinically referred to as detrusor overactivity, is a pathophysiological state defined by involuntary contractions of the bladder's detrusor muscle during the storage phase (StatPearls, 'Detrusor Overactivity'). This condition is the underlying cause of overactive bladder (OAB) syndrome, manifesting as urinary urgency, frequency, and urge incontinence (PubMed, PMID: 30135205). The hyperreactivity can stem from neurogenic causes, such as stroke or Parkinson's disease, or myogenic changes in the smooth muscle cells themselves (NIH, 'Overactive Bladder'). Pharmacological management targets the autonomic control of the bladder, specifically inhibiting the parasympathetic-mediated contraction via muscarinic M3 receptor antagonists or enhancing sympathetic-mediated relaxation via beta-3 adrenergic receptor agonists (Journal of Urology, 2024). Common drugs used to treat this condition include solifenacin and mirabegron, which act on these respective pathways to improve bladder capacity and reduce urgency (PubMed, PMID: 24581778). In refractory cases, onabotulinumtoxinA may be injected directly into the detrusor muscle to inhibit acetylcholine release (NIH, 'Botulinum Toxin'). Because it describes a physiological dysfunction rather than a specific protein, it is considered a clinical phenotype rather than a discrete molecular target.

Other names

Detrusor overactivityDetrusor hyperreflexiaOveractive bladderBladder overactivityInvoluntary detrusor contractions

Competitive antagonism of muscarinic M3 receptors to inhibit acetylcholine-induced bladder contraction; Agonism of beta-3 adrenergic receptors to increase cyclic AMP and promote detrusor relaxation; Proteolysis of SNAP-25 by botulinum toxin to prevent neurotransmitter release (StatPearls, 'Antimuscarinic Drugs'; PubMed, PMID: 24581778).