Effects of nitric oxide on pain perception by primary afferent neurons in inflammation

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In primary cultured trigeminal ganglion cells, NOC12, a nitric oxide (NO) donor, potentiated bradykinin (BK)-induced increase in intracellular free calcium concentration ([Ca^<2+>]i). The effect of NOC12 was blocked by carboxy-PTIO (specific NO radical scavenger) and ODQ (guanylate cyclase inhibitor), but not super oxide dismutase. 8-Bromo-cGMP potentiated the rise of [Ca^<2+>]i induced by BK.Both NOC12 and 8-bromo-cGMP did not affect the increase in [Ca^<2+>]i by histamine and carbachol. These results indicate that NO potentiates BK-induced increase in [Ca^<2+>]i by the activation of guanylate cyclase. This also suggests that NO may affect BK-mediated nociceptive responses.We investigated the effect of NO on kaolin-induced writhing behavior mediated by BK receptors. Intraperitoneal administration of lipopolysaccharide (LPS) in mice increase kaolin-induced writhing reaction, which was inhibited by BK-B2 receptor agonist Hoe140. The increase was inhibited by 2-iminopiperidine, an inducible NO synthase inhibitor. LPS-activated macrophages produced NO in a dose- and time-dependent manner. Pretreatment with 2-iminopiperidine caused a reduction in LPS-stimulated production of NO by peritoneal macrophages. These results indicate that LPS potentiated kaolin-induced writhing through producing NO.These results suggest that nitric oxide may potentiate pain perception in inflammation.