PGE1 [745-65-3] and PGE2 [363-24-6], but not PGF2α [551-11-1], dose-dependently potentiated pain provoked by subliminal arterial doses of bradykinin (I) [58-82-2]; the potentiating doses of prostaglandins did not cause pain themselves.PGE1 was more potent than PGE2.Aspirin [50-78-2], phenylbutazone [50-33-9], indomethacin [53-86-1], and ibuprofen [15687-27-1] (200; 15 and 60; 5 and 20; and 25 and 100 mg/kg, i.p., resp.) inhibited I-induced pain, but even at higher doses did not inhibit pain produced by concomitant I and PGE1 (1.5 μg).Morphine-HCl [52-26-6] (8 mg/kg, s.c.) inhibited I-induced pain responses whether PGE1 was present or not.Amidopyrine [58-15-1] inhibited pain induced by I alone or with PGE1, but was less potent against the combination.PGE1 and PGE2, but not PGF2α, potentiated induction of pain when kinin and prostaglandin were arterially injected together.Thus, nonsteroidal antiinflammatory drugs may produce analgesia by preventing prostaglandin formation, and this may be distinguishable from other types of analgesia (e.g. from morphine).Amidopyrine may act in part on spinal or peripheral sites to prevent prostaglandin formation.