TY - JOUR
T1 - Central effects of histamine H2-receptor agonists and antagonists on nociception in the rat
AU - Netti, C.
AU - Guidobono, F.
AU - Sibilia, V.
AU - Villa, I.
AU - Cazzamalli, E.
AU - Pecile, A.
PY - 1988/5
Y1 - 1988/5
N2 - The effects of intracerebroventricular injection of histamine H2-receptor agonists (4-methylhistamine, 4-MeH; dimaprit, DIM), H2-antagonists (cimetidine, CIM; ranitidine, RAN; famotidine, FAM) and of the DIM chemical analogue SK&F 91487 on hot-plate latency in rats were examined. Both DIM (0.4-0.8 μmol/rat) and 4-MeH (0.4-0.8 μmol/rat) significantly enhanced the pain threshold, whereas SF&F 91487 (0.8 μmol/rat) had no effect, indicating that DIM antinociception is specifically due to its activity on histamine (HA) receptors. The H2-antagonists CIM (0.8 μmol/rat) and RAN (0.6 μmol/rat) also enhanced the pain threshold, while FAM (0.03 μmol/rat) did not modify pain latency. When injected before 4-MeH, FAM reduced the antinociceptive effect of 4-MeH. These findings suggest that the antinociceptive activity of CIM and RAN is not related to specific blockade of H2-receptors and that the activation of HA-H2-receptors is inhibitory to nociception.
AB - The effects of intracerebroventricular injection of histamine H2-receptor agonists (4-methylhistamine, 4-MeH; dimaprit, DIM), H2-antagonists (cimetidine, CIM; ranitidine, RAN; famotidine, FAM) and of the DIM chemical analogue SK&F 91487 on hot-plate latency in rats were examined. Both DIM (0.4-0.8 μmol/rat) and 4-MeH (0.4-0.8 μmol/rat) significantly enhanced the pain threshold, whereas SF&F 91487 (0.8 μmol/rat) had no effect, indicating that DIM antinociception is specifically due to its activity on histamine (HA) receptors. The H2-antagonists CIM (0.8 μmol/rat) and RAN (0.6 μmol/rat) also enhanced the pain threshold, while FAM (0.03 μmol/rat) did not modify pain latency. When injected before 4-MeH, FAM reduced the antinociceptive effect of 4-MeH. These findings suggest that the antinociceptive activity of CIM and RAN is not related to specific blockade of H2-receptors and that the activation of HA-H2-receptors is inhibitory to nociception.
UR - http://www.scopus.com/inward/record.url?scp=0023908528&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023908528&partnerID=8YFLogxK
U2 - 10.1007/BF02142554
DO - 10.1007/BF02142554
M3 - Article
C2 - 2899383
AN - SCOPUS:0023908528
VL - 23
SP - 247
EP - 249
JO - Inflammation Research
JF - Inflammation Research
SN - 1023-3830
IS - 3-4
ER -