Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Further evidence is reported on the influence exerted by capsaicin on the anaphylactic reaction evoked in actively sensitized guinea-pigs. In Herxheimer microshock induced by ovalbumin aerosol, pretreatment of animals with 100 micrograms/kg i.p. capsaicin prolonged the preconvulsion time when the drug was administered 3 h before antigen challenge. In contrast, the same dose of capsaicin injected 30 min before aerosol caused a shortening of latency of the respiratory symptomatology. The influence of the drug is no longer evident after 24 h. In "in vitro" experiments desensitization to capsaicin of tracheal preparations caused a reduction of histamine and SRS-A released during antigen challenge, in comparison to controls. Moreover, anaphylactic histamine release was increased in preparations perfused with 10(-8) M substance P. In conclusion, our findings confirm that neuropeptides may be involved in the pathogenesis of asthma by affecting release of mediators.
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PMID:Capsaicin and anaphylactic reactions in the guinea-pig airways. 169 70

Slow-reacting substance produced in anaphylaxis (SRS-A) increased resistance of the lungs to inflation in the guinea-pig in vivo and caused isolated preparations of its tracheobronchial muscle to contract. SRS-A also contracted human isolated bronchial muscle and some but not all preparations of rabbit trachea. Nonsteroid anti-inflammatory drugs, which antagonize bronchoconstriction induced by kinins, but not that by histamine, acetylcholine, 5-hydroxytryptamine, substance P, angiotensin or lung prostaglandin, also antagonized the bronchoconstrictor action of SRS-A. This antagonism resembled that of kinins in being surmounted by higher doses of agonist, in the potencies of active drugs and in the types of drugs which were inactive. However, receptors in guinea-pig tracheobronchial muscle for SRS-A seem to be distinct from those for bradykinin, since preparations of this muscle could become unresponsive to either agent in vivo and in vitro, while remaining responsive to the other.
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PMID:BRONCHOCONSTRICTOR ACTION AND ANTAGONISM OF A SLOW-REACTING SUBSTANCE FROM ANAPHYLAXIS OF GUINEA-PIG ISOLATED LUNG. 1420 95

Zaltoprofen, a propionic acid derivative of non-steroidal anti-inflammatory drugs (NSAIDs), was shown to have more powerful inhibitory effects to bradykinin (BK)-nociception than other NSAIDs. However, the molecular mechanisms underlying this potent analgesia are not yet fully understood. Here we attempted to clarify the molecular mechanism underlying zaltoprofen-induced analgesia on BK-induced nociception by a novel algogenic-induced paw flexion (APF) test in mice. The intraplantar (i.pl.) injection of zaltoprofen at 1nmol showed strong analgesic action on BK (i.pl.)-induced nociceptive flexor responses, whereas loxoprofen or its active metabolite loxoprofen-SRS did not. Zaltoprofen also inhibited the nociception induced by [Tyr8]-BK, a specific agonist of B2-type BK receptor, but did not affect the nociception by [Lys-des-Arg9]-BK, a specific agonist of B1-type BK receptor. However, zaltoprofen did not affect the substance P-induced nociception, which is mediated by common post-receptor signaling through nociceptive fibers with BK-ones. All these results suggest that NSAID zaltoprofen possesses novel anti-nociceptive mechanism, which inhibits B2-type BK receptor function in nerve endings.
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PMID:NSAID zaltoprofen possesses novel anti-nociceptive mechanism through blockage of B2-type bradykinin receptor in nerve endings. 1640 42