Involvement of the nitric oxide/CGMP/KATP pathway in antinociception induced by exercise in rats

Aims Physical exercise is responsible for increasing the nociceptive threshold The present study aimed to investigate the involvement of the nitric oxide/(C)GMP/K-ATP, pathway in antinociception induced by acute aerobic exercise (AAc) in rats Main methods Wistar rats performed exercise in a rodent treadmill, according to an AAc protocol The nociceptive threshold was measured by mechanical and thermal nociceptive tests (paw-withdrawal, tail-flick and face-flick) To investigate the involvement of the NO/(C)GMP/K-ATP, pathway the following nitric oxide synthase (NOS) unspecific and specific inhibitors were used N-nitro-L-arginine (NOArg). Aminoguanidine. N-5-(1-Iminoethyl)-L-ornithine dihydrocloride (L-NIO). N-omega-Propyl-L-arginine (L-NPA), guanylyl cyclase inhibitor, 1H-[1,2,4]oxidiazolo[4.3-a]quinoxalin-1-one (ODQ), and K-ATP channel blocker, Glybenclamide, all administered subcutaneously at a dose of 2 mg/kg 10 min before exercise started Plasma and cerebrospinal fluid (CSF) nitrite levels were determined by spectrophotometry Key findings In the paw-withdrawal, tail-flick and face-flick tests. the AAc protocol produced antinociception, which lasted for more than 15 min This effect was significantly reversed (P<0 05) by NOS specific and unspecific inhibitors, guanylyl cyclase inhibitor (ODQ) and K-ATP, channel blocker (Glybenclamide) Acute exercise was also responsible for increasing nitrite levels in both plasma and cerebrospinal fluid Significance Taken together, these results suggest that the NO/(C)GMP/K-ATP, pathway participates in antinociception induced by exercise (C) 2010 Elsevier Inc All rights reserved