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The effects of endogenously and exogenously induced nitric oxides on the nociperception of rats



The effects of endogenously and exogenously induced nitric oxides on the nociperception of rats



Yakhak Hoeji 45(1): 116-124, February



Nitric oxide is a labile, gaseous, broad spectrum second messenger that used in various tissues and cells. If it is induced by endogenously and exogenously in the neuronal cells, it is able to mediate analgesia or hyperalgesia at the periphery and in the spinal level respectively. This dual role of nitric oxide in the sensory system is very intriguing but has not been fully understood yet. In this experiment, acetylcholine (300 mug/paw), sodium nitroprusside (600 mug/paw), and L-arginine (300 mug/paw) represented antinociceptive effect to noxious topical stimulus, but pronociceptive responses followed by spinally application (20 mug/5 mul, 10 mug/3 mul, 500 mug/5 mul respectively). Calcium ion is critical element which activates nitric oxide synthase, therefore verapamil (300 mug/paw) and NOS inhibitor (20 mg/kg, L-NAME or L-NOArg) are injected into right hind paw (i.pl.). When verapamil is combined with NOS inhibitor, analgesic effects through NO-cGMP pathway are inhibited as compared with ACh alone. Diluted formalin (2.5%), when injected into rats' hind paw (0.05 ml), elicited a biphasic algesic responses and nitric oxide had an analgesic effect on both Adelta and C sensory nerve fibers which manipulate the phases respectively. Nitric oxides, which produced from constitutive nitric oxide synthase, activated cyclooxygenase-type I and then prostaglandins are produced from them. So, indomethacin and ibuprofen, inhibitors of COX1 enzyme, when pre-treated intraperitoneally (100 mg/kg) could reduce the hyperalgesic state. From these results, it is possible to imagine that the intrathecally administered NO donors expressed hyperalgesia through both long-term potentiation mechanism and arachidonic acid-prostaglandin cascade.

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