NITRIC-OXIDE SYNTHASE INHIBITION SELECTIVELY POTENTIATES SWIM STRESS ANTINOCICEPTION IN RATS

Since nitric oxide (NO) has been implicated in nociceptive processing, the present study examined whether NO synthase inhibition with either N-w-nitro-L-arginine (L-NA) or its methyl ester (L-NAME) would alter antinociception elicited by either continuous (CCWS) or intermittent c old-water swims (ICWS) on the tail-flick and jump tests. Whereas CCWS antinociception on both tests was significantly potentiated by a dose range of L-NA (0.1-4 mg/kg IF) and L-NAME (1 mg/kg IF), ICWS antinocic eption was largely unaffected by these manipulations. In contrast, adm inistration of the less active D isomer (D-NAME) failed to alter CCWS antinociception and reduced ICWS antinociception. The ability of NO sy nthase inhibition to potentiate CCWS antinociception could not be expl ained by changes in CCWS hypothermia. Since ICWS antinociception is me diated by p-opioid manipulations and CCWS antinociception is sensitive to delta-opioid and nonopioid manipulations, this indicates that NO s ynthase inhibition may be acting upon a selective form of pain inhibit ion.