Detrusor smooth muscle contractile machinery (DSM contractile machinery)

The detrusor smooth muscle (DSM) contractile machinery is the integrated system of proteins and signaling pathways responsible for the contraction and relaxation of the urinary bladder wall (Andersson & Arner, 2004). The primary mechanism involves the phosphorylation of the 20-kDa regulatory myosin light chain (LC20) by myosin light chain kinase (MLCK), which is activated by the calcium-calmodulin complex (Sellers & Chess-Williams, 2012). This process is countered by myosin light chain phosphatase (MLCP), which dephosphorylates LC20 to induce relaxation. The machinery is further regulated by calcium sensitization pathways, notably the RhoA/Rho-kinase (ROCK) and Protein Kinase C (PKC)/CPI-17 pathways, which inhibit MLCP activity, thereby maintaining contraction even at low calcium levels (Wuest et al., 2014). Dysregulation of these components is a hallmark of lower urinary tract symptoms (LUTS), including overactive bladder (OAB) and detrusor overactivity. Pharmacological intervention typically targets upstream receptors, such as muscarinic M3 receptors or beta-3 adrenergic receptors, or downstream effectors like ROCK to modulate bladder tone and voiding function (Woodcock et al., 2021).

Other names

Bladder smooth muscle contractile apparatusDetrusor myofilament complexDetrusor signaling pathways

Modulation of myosin light chain phosphorylation through inhibition of excitatory muscarinic signaling, activation of inhibitory adrenergic signaling, or direct inhibition of calcium-sensitizing enzymes like Rho-kinase.