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The urothelium modulates detrusor activity through releasing factors whose nature has not been clearly defined. Here we have investigated the involvement of H 2 S as possible mediator released downstream following muscarinic (M) activation, by using human bladder and urothelial T24 cell line. Carbachol stimulation enhances H 2 S production and in turn cGMP in human urothelium or in T24 cells. This effect is reversed by cysthationine-β-synthase (CBS) inhibition. The blockade of M1 and M3 receptors reverses the increase in H 2 S production in human urothelium. In T24 cells, the blockade of M1 receptor significantly reduces carbachol-induced H 2 S production. In the functional studies, the urothelium removal from human bladder strips leads to an increase in carbachol-induced contraction that is mimicked by CBS inhibition. Instead, the CSE blockade does not significantly affect carbachol-induced contraction. The increase in H 2 S production and in turn of cGMP is driven by CBS-cGMP/PKG-dependent phosphorylation at Ser 227  following carbachol stimulation. The finding of the presence of this crosstalk between the cGMP/PKG and H 2 S pathway downstream to the M1/M3 receptor in the human urothelium further implies a key role for H 2 S in bladder physiopathology. Thus, the modulation of the H 2 S pathway can represent a feasible therapeutic target to develop drugs for bladder disorders.

Urothelium muscarinic activation phosphorylates CBSSer227 via cGMP/PKG pathway causing human bladder relaxation through H2S production