Linked Life Data

7687291

Source:http://linkedlifedata.com/resource/pubmed/id/7687291

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-8-19
pubmed:abstractText
The increase in tracheal vascular permeability evoked by hypertonic saline depends on capsaicin-sensitive sensory nerves, which contain substance P and other neuropeptides. The present study was performed to determine whether a novel, nonpeptide, selective antagonist of the NK1 tachykinin receptor CP-99,994, [(+)-(2S-3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine], can prevent the effect of substance P, capsaicin and hypertonic saline on tracheal vascular permeability. CP-99,994 was also tested against a nonpeptide inflammatory mediator, platelet-activating factor (PAF), to assess the selectivity of its action. Anesthetized F-344 rats were injected with either substance P (5 micrograms/kg i.v.), capsaicin (100 micrograms/kg i.v.) or PAF (10 micrograms/kg i.v.), or were exposed to ultrasonically nebulized 3.6% NaCl. In each group, some of the rats were pretreated with CP-99,994 (1 to 4 mg/kg i.v.), and some with its vehicle (0.9% NaCl). Groups of rats injected with substance P or exposed to hypertonic saline were pretreated with the (2R, 3R)-enantiomer CP-100,263, [(-)-(2R-3R)-3-(2-methoxybenzylamino)-2-phenylpiperidine] (2 or 4 mg/kg i.v.). The magnitude of the increase in tracheal vascular permeability was measured by quantifying the extravasation of Evans blue dye. CP-99,994 prevented the increase in tracheal vascular permeability produced by inhalation of hypertonic saline, by substance P and by capsaicin, but did not prevent the effect of PAF. CP-100,263 did not affect substance P- and hypertonic saline-induced increase in vascular permeability. These results indicate that the NK1 receptor antagonist CP-99,994 produces stereoselective inhibition of neurogenic plasma extravasation evoked by inhalation of hypertonic saline.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
270-3
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7687291-Animals, pubmed-meshheading:7687291-Capillary Permeability, pubmed-meshheading:7687291-Capsaicin, pubmed-meshheading:7687291-Dose-Response Relationship, Drug, pubmed-meshheading:7687291-Edema, pubmed-meshheading:7687291-Evans Blue, pubmed-meshheading:7687291-Extravasation of Diagnostic and Therapeutic Materials, pubmed-meshheading:7687291-Hypertonic Solutions, pubmed-meshheading:7687291-Neurokinin A, pubmed-meshheading:7687291-Neurons, Afferent, pubmed-meshheading:7687291-Piperidines, pubmed-meshheading:7687291-Platelet Activating Factor, pubmed-meshheading:7687291-Rats, pubmed-meshheading:7687291-Rats, Inbred F344, pubmed-meshheading:7687291-Receptors, Neurotransmitter, pubmed-meshheading:7687291-Receptors, Tachykinin, pubmed-meshheading:7687291-Sodium Chloride, pubmed-meshheading:7687291-Stimulation, Chemical, pubmed-meshheading:7687291-Substance P, pubmed-meshheading:7687291-Trachea, pubmed-meshheading:7687291-Tracheal Diseases
pubmed:year
1993
pubmed:articleTitle
A new NK1 receptor antagonist (CP-99,994) prevents the increase in tracheal vascular permeability produced by hypertonic saline.
pubmed:affiliation
Cardiovascular Research Institute, University of California, San Francisco.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't