High impact information on Rpr 100893

• Daily administration by gastric intubation of 1 mg/kg or 10 mg/kg of the NK1 receptor antagonist (RPR 100893) leads to detectable levels of the antagonist in the blood of treated animals for at least 6 hr after its administration [1].
• The non-peptide neurokinin-1 antagonist, RPR 100893, decreases c-fos expression in trigeminal nucleus caudalis following noxious chemical meningeal stimulation [2].
• The effect of RPR 100893, a selective and specific neurokinin-1 antagonist, or its enantiomer RPR 103253 was examined on c-fos antigen expression in brain stem and upper cervical cord 2 h after intracisternal capsaicin injection (30.5 micrograms/ml) in pentobarbital-anesthetized Hartley guinea-pigs [2].
• Pretreatment with RPR 100893 (1, 10 and 100 micrograms/kg, i.v.) but not its enantiomer (100 micrograms/kg, i.v.) 30 min prior to capsaicin injection significantly reduced the number of positive cells in the trigeminal nucleus caudalis (P < 0.01) in a dose-dependent manner, but not within area postrema or nucleus of the solitary tract [2].
• 3. When given i.v. 30 min prior to electrical stimulation, RPR 100893 (> or = 0.5 ng kg-1) significantly inhibited plasma protein extravasation in the dura mater evoked by electrical stimulation in a dose-dependent manner [3].

Anatomical context of Rpr 100893

• Blockade by oral or parenteral RPR 100893 (a non-peptide NK1 receptor antagonist) of neurogenic plasma protein extravasation within guinea-pig dura mater and conjunctiva [3].

Gene context of Rpr 100893

• Effects of RPR 100893, a potent NK1 antagonist, on the jaw-opening reflex in the guinea pig [4].

References