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. 2020 May;373(2):214–219. doi: 10.1124/jpet.119.264697

Fig. 4.

Fig. 4.

Proposed mechanism of NO-np action on amelioration of detrusor overactivity in the SCD mouse. The molecular mechanism underlying detrusor overactivity in the SCD mouse involves the reduction in Akt/eNOS activities (reduced phosphorylation of Akt on Ser-473 and eNOS on Ser-1177) and increased RhoA/ROCK contractile pathway (increased phosphorylation of MYPT1, a regulatory subunit of MLCP, on Thr-696). NO-np treatment increases Akt/eNOS activities and decreases RhoA/ROCK activity in the SCD mouse bladder by enhancing blood flow and shear forces on the urothelium. Decreased phosphorylation of MYPT1 activates MLCP, which dephosphorylates the MLC and initiates relaxation of smooth muscles. Normalized Akt/eNOS and RhoA/ROCK activities ameliorate detrusor overactivity. MLC, myosin light chain; MLCK, myosin light chain kinase; MLCP, myosin light chain phosphatase.