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• W3094423021 startingPage "753" @default.
• W3094423021 abstract "The aim of this study was to examine if the peripheral antinociceptive effects of the opioid agonist/antagonist nalbuphine and buprenorphine involve the sequential participation of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) synthesis followed by K + channel opening in the formalin test. Wistar rats (180–220 g) were injected in the dorsal surface of the right hind paw with formalin (1%). Rats received a subcutaneous (s.c.) injection into the dorsal surface of the paw of vehicles or increasing doses of nalbuphine (50–200 μg/paw) or buprenorphine (1–5 μg/paw) 20 min before formalin injection into the paw. Nalbuphine antinociception was reversed by the s.c. injection into the paw of the inhibitor of NO synthesis (N G -nitro-l-arginine methyl ester (L-NAME)), by the inhibitor of guanylyl cyclase (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ)), by the K ir 6.1–2, ATP-sensitive K + channel inhibitors (glibenclamide and glipizide), by the K Ca 2.1–3, small conductance Ca 2+ -activated K + channel blocker (apamin), by the K Ca 1.1, large conductance Ca 2+ -activated K + channel blocker (charybdotoxin), and by the K V , voltage-dependent K + channel inhibitors (4-aminopyridine (4-AP) and tetraethylammonium chloride (TEA)). The antinociceptive effect produced by buprenorphine was blocked by the s.c. injection of 4-AP and TEA but not by L-NAME, ODQ, glibenclamide, glipizide, apamin, or charybdotoxin. The present results provide evidence for differences in peripheral mechanisms of action between these opioid drugs." @default.
• W3094423021 created "2020-10-29" @default.
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• W3094423021 date "2020-11-01" @default.
• W3094423021 modified "2023-09-29" @default.
• W3094423021 title "Participation of the opioid receptor – nitric oxide – cGMP – K⁺channel pathway in the peripheral antinociceptive effect of nalbuphine and buprenorphine in rats" @default.
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• W3094423021 doi "https://doi.org/10.1139/cjpp-2020-0104" @default.
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