The role and interaction of hydrogen sulfide and reactive oxygen species in the disruption of agonist-induced contractile responses in a mouse model of cyclophosphamide-induced cystitis.

Interstitial cystitis is a syndrome characterized by sensory and motor dysfunction of the lower urinary tract. Hydrogen sulfide is an endogenously produced gasotransmitter and is responsible for regulating many functions. In this thesis, the effect of urothelium tissue in the bladder on agonist induced contractile responses in an acute cystitis mouse model obtained by intraperitoneally administered cyclophosphamide, as well as the roles and interaction of hydrogen sulfide and reactive oxygen derivatives scavengers in cystitis were investigated. In the bladder tissue having cystitis, carbachol-induced contractile responses were increased and the functions of the urothelium was deteriorated. Besides, carbachol-induced cumulative contractile responses in detrusor smooth muscle tissues with urothelium in cystitis group were not altered by catalase, superoxide dismutase and N-acetyl cysteine, but inhibited by NaHS. Moreover, in urothelium denuded bladder detrusor strips, maximum contractile response induced by carbachol was decreased by catalase and NaHS. The results obtained are important in terms of understanding the pathophysiological effects of cystitis in the bladder and developing new treatment targets.