In a rat study, bladder inflammation pain was shown to be induced by anandamide via TRPV1. This proposes that TRPV1 may be used as a therapeutic target (Dinis et al., 2004).
On the contrary, by increasing the level of anandamide through inhibiting its breakdown by FAAH, potent analgesic and anti-inflammatory effects have been observed (Wang et al., 2015).
In a study with female rats, upon induction of cystitis with cyclophosphamide, an increase was found in PEA and CB1, PPARα was decreased and CB2 was unaffected (Pessina et al., 2014). PEA was found to reduce pain and bladder voiding. CB1 and PPARα antagonists blocked this effect.
Several studies observed that CB2 was found to be increased with cystitis (Merriam et al., 2008; Tambaro et al., 2014) and that stimulation of CB2 with PEA or anandamide reduced pain and inflammation (Jaggar et al., 1998; Wang et al., 2013, 2014).
Acetylcholine-induced contractions in the bladder were shown to be reduced by CBG, proposing a potential effect in treating bladder disorders (Pagano et al., 2015).