Fidecka S, Lalewicz S
Department of Pharmacodynamics, Medical Academy, Lublin, Poland.
Pol J Pharmacol. 1997 Nov-Dec;49(6):395-400.
The participation of nitric oxide (NO) in antinociceptive activity of molsidomine and sodium nitroprusside (SNP) was studied in mice using the writhing test. Molsidomine (300 and 150 mg/kg) and SNP (1.52-0.38 mg/kg) induced antinociception that was antagonized by naloxone. L-arginine (500-62.5 mg/kg) did not produce antinociceptive effects, whereas N omega-nitro-L-arginine methyl ester (L-NAME) (37.5-150 mg/kg) induced antinociception which was suppressed by naloxone. Methylene blue did not change the molsidomine- and SNP-induced antinociception, but significantly intensified that produced by L-NAME. L-arginine increased antinociceptive effect of molsidomine but not that of SNP. Antinociceptive activity of L-NAME was partially reversed by L-arginine. D-arginine failed to influence these effects. The present findings suggest that the NO-cGMP pathway is not involved in the mechanism of molsidomine- and SNP-induced antinociception in the writhing test in mice.
采用扭体试验，在小鼠中研究了一氧化氮（NO）参与吗多明和硝普钠（SNP）的抗伤害感受活性。吗多明（300和150mg/kg）和SNP（1.52 - 0.38mg/kg）诱导的抗伤害感受可被纳洛酮拮抗。L-精氨酸（500 - 62.5mg/kg）未产生抗伤害感受作用，而Nω-硝基-L-精氨酸甲酯（L-NAME）（37.5 - 150mg/kg）诱导的抗伤害感受可被纳洛酮抑制。亚甲蓝未改变吗多明和SNP诱导的抗伤害感受，但显著增强了L-NAME产生的抗伤害感受。L-精氨酸增加了吗多明的抗伤害感受作用，但未增加SNP的抗伤害感受作用。L-精氨酸部分逆转了L-NAME的抗伤害感受活性。D-精氨酸未能影响这些作用。目前的研究结果表明，在小鼠扭体试验中，NO - cGMP途径不参与吗多明和SNP诱导的抗伤害感受机制。
