Neurogenic Inflammation In the nasal mucosa is cause by neuropeptides such as substance P, released from sensory nerve endings. The effects of substance P are decreased by neutral endopeptidase(NEP), which is a peptidase that degrades substance P and other sensory neuropeptides. In this present study, we used capsaicin(100μg/kg iv) to produce neurogenic inflammation in the septal mucosa of rats, and we examined the effect of phosphoramidon(2.5mg/kg iv) in neurogenic inflammation(vascular permeability). Sites of increased vascular permeability were localized with Monastral bule. In rats that received Monastral blue alone, no extravasated blood vessels were found in the septal mucosa, whereas capsaicin or phosphoramidin alone caused only slight extravasation of Monastral blue pigment in the anterior septal mucosa(3.04±0.81mm/0.2mm² vs 1.51±0.65mm/0.2mm²). When the phosphoramidon was followed by the capsaicin, many venules were labelled with Monastral blue(7.22±1.89mm/0.2mm²). On the other hand, when the vehicle was preceeded by phosphoranidon, a few venules were lavelled in the anterior septal mucosa(1.29±0.71mm/0.2mm²). We conclude that decreased NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentration of substance P to reach tachykinin receptor in the nasal mucosa. Thus decreased NEP activity may exacerbate some of the pathologic response in the nasal mucosa.