Verify the role of the kinin B₁ receptors (B₁R) and the effect of ACE inhibitors (ACEi) on acute gout induced by monosodium urate (MSU) crystals in rodents.

Painful (overt pain and allodynia) and inflammatory parameters (joint oedema, leukocyte trafficking, interleukin-1β levels) of acute gout attacks were assessed several hours after an intra-articular injection of MSU (1.25 or 0.5 mg/articulation) into the ankle of rats or mice, respectively. The role of B₁R was investigated using pharmacological antagonism or gene deletion. Additionally, B₁R immunoreactivity in ankle tissue and sensory neurons, kininase I activity and des-Arg⁹-bradykinin synovial levels were also measured. Similar tools were used to investigate the effects of ACEi on a low dose of MSU (0.0125 mg/articulation)-induced inflammation.

Kinin B₁R antagonism or gene deletion largely reduced all painful and inflammatory signs of gout. Furthermore, MSU increased B₁R expression in articular tissues, the content of the B₁ agonist des-Arg⁹-bradykinin and the activity of the B₁ agonist-forming enzyme kininase I. A low dose of MSU crystals, which did not induce inflammation in control animals, caused signs of acute gout attacks in ACEi-treated animals that were B₁R-dependent.

Kinin B₁R contributes to acute gouty attacks, including the ones facilitated by ACEi. Therefore, B₁R is a potential therapeutic target for the treatment and prophylaxis of gout, especially in patients taking ACEi.