Beta-3 adrenoreceptor agonists act directly to inhibit afferent nerve firing independent of the relaxing effects on the bladder smooth muscle.
Anticholinergic agents are thought to act primarily by inhibiting involuntary detrusor muscle contractions (at the level of the efferent pathway), but identification of muscarinic receptors in the urothelium/suburothelium suggests that they may also affect the afferent sensory pathway.
Most of the effects of onabotulinumtoxinA are thought to be the result of inhibition of the release of acetylcholine from the presynaptic nerve terminal, which prevents stimulation of the detrusor muscle. Clinical data show a profound effect of botulinum toxin on involuntary detrusor contractions and elevated detrusor pressures. Botulinum neurotoxin type A may also affect other neurotransmitters, such as sensory/afferent neurotransmitters.
Tricyclic antidepressants, such as imipramine and doxepin, have been used to treat OAB. These block the reuptake of noradrenaline and serotonin. However, whether this mechanism mediates the beneficial effects on bladder hyperactivity is unclear. Tricyclic antidepressants are not recognized as first-line therapy for the treatment of OAB.
Learn more about beta3-receptor agonists in the management of OAB.
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Cite this: Bradley Schwartz. Fast Five Quiz: Overactive Bladder Pharmacologic Management - Medscape - Feb 26, 2021.