The contribution of nitric oxide (NO) to articular pain in arthritis induced by zymosan (1 mg, intra articular) in rats was assessed by measuring articular incapacitation (AI). Systemic treatment with the non‐selective NO synthase (NOS) inhibitor L‐NAME (10–100 mg kg−1 i.p.) or with the selective iNOS inhibitors aminoguanidine (AG; 10–100 mg kg−1 i.p.) or 1400W (0.5–1 mg kg−1 s.c.) inhibited the AI induced by injection of zymosan 30 min later. Local (intra articular) treatment with the NOS inhibitors (L‐NAME or AG, 0.1–1 μmol; 1400W, 0.01 (μmol) 30 min before zymosan also inhibited the AI. Systemic or local treatment with the NOS inhibibitors (L‐NAME; AG, 100 mg kg−1 i.p. or 0.1 μmol joint−1; 1400W, 1 mg kg−1 s.c. or 0.01 μmol joint−1), 2 h after zymosan did not affect the subsequent AI. Local treatment with the NO donors SNP or SIN‐1, 2 h after zymosan did inhibit AI. L‐NAME and AG, given i.p. inhibited nitrite but not prostaglandin E2 (PGE2) levels in the joints. L‐NAME (100 mg kg−1) but not AG (100 mg kg−1) increased mean arterial blood pressure. Neither L‐NAME, AG nor the NO donor SIN‐1 altered articular oedema induced by zymosan. In conclusion, inhibitors of iNOS decrease pain in zymosan arthritis only when given before the zymosan. This was not due to inhibition of articular PGE2 release or oedema. NO donors also promoted antinociception in zymosan arthritis without affecting oedema. British Journal of Pharmacology (2002) 136, 588–596; doi:

in the cell influx (CI) and the articular incapacitation (AI) in the zymosan induced-arthritis (ZyA

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