Abstract

Acetylcholine released from nerves mediates smooth muscle contraction of the bladder. This contractile response is primarily mediated by the M3 receptor subtype in most smooth muscles, including the bladder. Anticholinergics are one of the primary treatments for overactive bladder. The target for these anticholinergics may be muscarinic receptors in the detrusor muscle, the urothelial layer, or even presynaptic nerves. This review focuses on the alteration in the function of the various muscarinic receptor subtypes that are important for bladder function seen in various pathophysiologic conditions or experimental pathologies developed in animal models. These alterations may affect the efficacy of anticholinergic treatment in some patients.

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