Schematic representation of nitric oxide release and its effects in the urinary bladder wall. Mechanical stretch (1) or activation of vanilloid receptors (2) can cause release of nitric oxide from the urothelium. Mechanically induced release seems to be dependent on the presence of vanilloid receptors (1). Activation of muscarinic receptors (3) or beta-adrenoceptors (4) can cause release of nitric oxide from the urothelium, affecting detrusor contractility directly or indirectly by modulating the activity of afferent nerve terminals located in the lamina propria. While nitric oxide formed from eNOS has been shown to increase urothelial barrier function (5), desensitize afferent nerve terminals (6) and attenuate detrusor contractility (7), nitric oxide formed from iNOS has been shown to cause disruption of barrier function (5), sensitize afferent nerve terminals (6), and facilitate bladder contraction (7).
