**3.1 Prostaglandins**

Prostanoids (prostaglandins and thromboxanes) are synthesized by cyclo-oxygenase (COX), present in several tissues including the bladder wall (Khan et al., 1998; Lecci et al., 2000; Azadzoi et al., 2003; Andersson & Wein, 2004). Two COX isoforms exist. COX-1 is expressed constitutively and participates in normal bladder function whereas COX-2 is activated during cystitis (Lecci et al., 2000; Tramontana et al., 2000). Prostanoid synthesis can be induced by physiological stimuli (for example, detrusor muscle stretching), injuries of the mucosa, nerve stimulation, ATP and inflammatory mediators such as bradykinin and the chemotactic peptide N-formyl-l-methionyl-l-leucyl-l-phenylalanine (Khan et al., 1998; Andersson & Wein, 2004).

Prostaglandin (PG) E2 is one the most abundant prostanoid in the bladder (Jeremy et al., 1987; Khan et al., 1998). In rats, intravesical administration of PGE2 facilitates micturition, increases basal intravesical pressure and induces bladder hyperactivity (Ishizuka et al., 1995). In the urethra, topical application of PGE2 causes relaxation of the sphincter (Yokoyama et al., 2007). Likewise, intravesical instillation of an inhibitor of the COX-2 enzyme improved bladder function in an animal model of OAB (Jang et al., 2006). This supports a role for this prostanoid during bladder dysfunction and has justified a few inconclusive clinical trials regarding the use of non-steroidal anti-inflammatory drugs in the treatment of OAB. So, expectations were raised when Kim and co-workers found that levels of PGE2 and PGF2α were significantly higher in male and female OAB patients that in healthy controls (Kim et al., 2005; Kim et al., 2006). However, PG concentrations were not corrected for urine concentration. After correction for creatinine values, Liu and co-workers found no significant differences in PGE2 content in patients with OAB wet, OAB dry and controls (Liu et al., 2010).

Thus, at this moment the role of urinary PGs, most notably PGE2, as a putative tool for OAB diagnosis and follow-up is highly debatable. Moreover, the measuring methods rely on labour-intensive and expensive laboratory procedures. In addition, although it is relatively consensual that prostanoids participate in the mechanisms of OAB, it is not known if the recommended OAB therapies effectively reduce the PGs levels.
