Neurogenic oedema and vasodilatation
| Autor: | P K. Moore, S D. Brain, P K. Towler, G S. Bennett |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Male
Hydrocarbons Fluorinated Neuropeptide Vasodilation Substance P Nitric Oxide Synthase Type I Calcitonin gene-related peptide Pharmacology Arginine chemistry.chemical_compound Phenols medicine Animals Edema Vasoconstrictor Agents Peripheral Nerves Enzyme Inhibitors Rats Wistar Inflammation Neurogenic inflammation biology General Neuroscience Imidazoles Electric Stimulation Hindlimb Rats Nitric oxide synthase medicine.anatomical_structure chemistry Enzyme inhibitor Anesthesia biology.protein Nitric Oxide Synthase Sensory nerve |
| Zdroj: | NeuroReport. 9:1513-1518 |
| ISSN: | 0959-4965 |
| DOI: | 10.1097/00001756-199805110-00049 |
| Popis: | The effects of a neuronal nitric oxide synthase (nNOS) inhibitor, 1-(2-trifluoromethylphenyl)imidazole (TRIM) on rat sensory saphenous nerve-induced neurogenic inflammation were investigated. TRIM (50 mg kg-1, i.p.), but not 2-trifluoromethylphenol (TRIMPOH) which lacks nNOS inhibitory activity, inhibited neurogenic oedema by 55.8 +/- 6.5% (n = 6, p < 0.05). The effect of TRIM was partially reversed by L-arginine (100 mg kg-1, i.v., p < 0.01). TRIM also caused a reduction (p < 0.05) in neurogenic vasodilatation but had no effect on neuropeptide responses induced by substance P + CGRP. Topically applied TRIM (100 microliters of 150-250 mg ml-1) inhibited neurogenic oedema (p < 0.01). Thus, use of this recently described nNOS inhibitor has provided new evidence to further the hypothesis that nNOS plays a role in modulating sensory nerve-mediated neurogenic inflammation. |
| Databáze: | OpenAIRE |
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