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

Substance P was examined for sneeze-inducing activity and its involvement of sneeze responses in experimental allergic rhinitis. Substance P, dripped into a nostril of guinea pigs, at concentrations of 100 pM and above induced sneezing in a dose-dependent fashion. The activity of substance P was not affected by the previous subcutaneous injections of capsaicin that depleted substance P in nerve fibers. Histamine induced sneezing at concentrations of 30 mM and above and the activity was reduced by capsaicin treatment. The frequency of antigen-induced sneezing was proportional to the substance P content in nasal mucosa of sensitized guinea pigs treated with increasing doses of capsaicin; correlation coefficient 0.91. These results suggest that substance P plays an important role as a stimulator of sneeze responses in experimental allergic rhinitis in guinea pigs.
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PMID:Substance P as a potent stimulator of sneeze responses in experimental allergic rhinitis of guinea pigs. 128 91

To elucidate the effect of capsaicin-sensitive nerve fibers, which are known to contain substance P (SP) and other sensory neuropeptides, on the sneezing reflex, we have investigated the effect of capsaicin on this reflex provoked in guinea pigs passively sensitized with anaphylactic antibody followed by specific antigen challenge. It has already been established that histamine released from mast cells is a reliable inducer of the sneezing reflex in type I allergy. Our experimental results indicated that the frequency of sneezing provoked by antigen challenge as well as histamine application was significantly reduced by pretreatment with capsaicin in a dose-dependent fashion. SP is considered to be one of the main neurotransmitters in sensory nerves. When the amount of SP in animal nasal mucosa was measured 12 h after capsaicin treatment, a marked reduction was noted. However, the histamine content in the nasal mucosa was not changed by capsaicin treatment. These data suggest that neuropeptides, especially SP, which are released or depleted from sensory nerves by capsaicin treatment, probably play an important role as neurotransmitters of the stimulant histamine in the development of sneezing in type I allergy.
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PMID:Effect of capsaicin as a neuropeptide-releasing substance on sneezing reflex in a type I allergic animal model. 138 48

The major pathological changes in rhinitis are vascular, with blood sinus congestion, transudation and oedema, and glandular, with mucus secretion. Both block the nose. Mediators released by antigen-antibody reactions and by inflammatory processes will disrupt nasal function in three main ways. First, mediators such as histamine, bradykinin and leukotrienes will act directly on blood vessels and submucosal glands, causing mucosal thickening and secretion. Second, the same mediators will excite terminals of sensory nervous receptors in the nose, setting up axon reflexes with release of neuropeptides from other branches of the nervous receptors. Neurokinins, such as substance P, will augment vasodilatation and transudation and may modulate the secretions from submucosal glands. Third, the same sensory receptors when stimulated will set up central nervous reflex actions. The responses include sneezing and nasal irritation (both prominent features of rhinitis) reflex nasal vasodilatation and mucus secretion, and actions on the lower airways. The relative importance of these three mechanisms is difficult to assess in man. Successful therapy may act by preventing one of the undesirable motor constituents of rhinitis, or may have a more general action in lessening inflammation or immunological responses.
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PMID:Nasal pathophysiology. 228 93

Local and systemic capsaicin pretreatment as well cryosurgery induced a long-lasting loss of sensory substance P-immunoreactive nerves in the guinea-pig nasal mucosa. In addition, cryosurgery caused a loss of noradrenergic sympathetic nerves, sclerosis of blood vessels, epithelial damage and fibrosis of the mucosa. The sneezing response to local application of capsaicin--but not that to nicotine--was reduced or abolished by capsaicin pretreatment and cryosurgery, while the response to tactile stimulation was unaffected. These effects were long-lasting and still present 2 months after treatment. Local capsaicin pretreatment of the nasal mucosa had no effects on the substance P levels or the Evans Blue extravasation response to i.v. capsaicin in the ureter, indicating that this treatment has no systemic effects on other afferent SP-neurons. It is suggested that local capsaicin pretreatment is a more selective and less traumatic method than cryosurgery to induce a long-lasting desensitization of the nasal mucosa to chemical irritants in hyperreactive disorders of the nose.
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PMID:Effects of nasal capsaicin pretreatment and cryosurgery on sneezing reflexes, neurogenic plasma extravasation, sensory and sympathetic neurons. 241 Oct 99

The term hyper-reactivity defines an inadequate reaction of the nose to normal airborne stimuli that are harmless to most of the population. In such cases the nose always shows exactly the same symptoms, irrespective of whether the rhinitis is allergic (IgE- or cell-mediated) or nonspecific (vasomotor). These symptoms include sneezing, nasal obstruction, hypersecretion, and itching of the nose. The vascular supply of the nose consists of capacitance vessels (veins, venules, sinusoids), resistance vessels (arteries, arterioles), and exchange vessels (capillaries of fenestrated types). Drug and mediator effects may be directed to different nasal vessel systems. The autonomic innervation of the nose is complex. Some neuropeptides have been demonstrated, in addition to the classical neurotransmitters of the sympathetic and parasympathetic system. Neuropeptide Y (NPY) is found in adrenergic fibers, vasoactive intestinal peptide (VIP) in cholinergic neurones; substance P (SP), calcitonin-gene-related peptide (CGRP) and neurokinine (NKA) are found in sensory nerves. The possible significance of the different neurotransmitters and mediators in nasal hyperreactivity is discussed.
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PMID:[Current aspects of nasal hyperreactivity]. 306 18

1. Topical application of capsaicin to the human nasal mucosa induced a burning sensation and sneezing. A dose-dependent seromucous nasal secretion was also observed. Capsaicin (75 micrograms) was more potent than methacholine (50 mg) in producing nasal secretion, while topical histamine (200 micrograms), substance P (135 micrograms) and calcitonin gene-related peptide (36 micrograms) did not induce rhinorrhea. 2. Pretreatment with either topical ipratropium bromide, systemic dexchlorpheniramine or indomethacin did not influence the effects induced by capsaicin. Topical pretreatment with lidocaine inhibited the painful sensation but failed to block the rhinorrhea. Desensitization to the effects of capsaicin occurred following 4-5 subsequent applications, and full recovery was observed within 30-40 days. 3. It is proposed that the effects of capsaicin in human nasal mucosa are due to excitation of primary afferent neurones that (a) convey burning and painful sensation, (b) evoke a sneezing reflex and (c) induce nasal secretion by releasing transmitter(s) from their peripheral terminals.
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PMID:Secretion, pain and sneezing induced by the application of capsaicin to the nasal mucosa in man. 337 Mar 86

The role of neuropeptides in nasal hyperreactivity was examined in guinea pigs by histochemical and pharmacological study. Intranasal application of toluene diisocynate (TDI) induced nasal hyperreactivity symptoms: sneezing and watery rhinorrhea, and decreased histamine content in the nasal mucosa in guinea pigs sensitized with TDI. The immunoreactivity of substance P (SP) and calcitonin gene-related peptide (CGRP) in the nerve terminals in the nasal mucosa was increased after intranasal application of TDI. We also observed a decrease in the immunoreactivity of SP and CGRP, and an increase in their mRNA expression in trigeminal ganglion neurons. These findings indicate that exposure to TDI enhanced the biosynthesis of both SP and CGRP in the trigeminal ganglion neurons and their axonal transportation to the terminals in the nasal mucosa. In animals pretreated with capsaicin before sensitization, TDI did not induce nasal allergy-like behavior and histamine release in the nasal mucosa. Since capsaicin depletes SP and CGRP in the sensory nerves, this finding indicates neuropeptide-mediated histamine release in the nasal mucosa. All these findings suggest that, on exposure to TDI, the antidromic release of SP and CGRP in the nasal mucosa triggers the release of histamine, resulting in the development of symptom of nasal hyperreactivity.
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PMID:[Neurogenic inflammation in nasal hyperreactivity]. 751 48

Experimental guinea pigs with allergic rhinitis were treated with capsaicin (CAP). During the whole course of treatment, nasal secretions, sneezing and nasal scratching were observed and recorded, as compared quantitatively with those of the control group. By means of specific radioimmunoassay, determination of the amount of substance P (SP) in the nasal mucosa was done in the treated group, untreated group and normal control group. By using the filter paper technique, the functional status of the nasal secretion was observed. The experimental group was given CAP by dripping into the nasal cavities for 15 days. The results indicated that the various symptoms of allergic rhinitis were obviously relieved. The nasal secretions were decreased by 64% as compared with those before the treatment; and SP content in the nasal mucosa was remarkably reduced in comparison with untreated group. The results of the experiment indicated: the repeated use of CAP might effectively deplete SP content in the nasal mucosa and prove the new theory of the effects of CAP on the desensitization of the SP nerves. CAP as a blocking agent of SP nerves blocked the axon reflex and exerted curative effect on allergic rhinitis.
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PMID:[Experimental study on blocking agent of substance P nerves in the treatment of allergic rhinitis]. 753 31

The role of neuropeptides in nasal allergy was examined in guinea pigs by histochemical and pharmacological study. Intranasal application of toluene diisocyanate (TDI) induced nasal allergy-like behaviors: sneezing and watery rhinorrhea, and decreased histamine content in the nasal mucosa in guinea pigs sensitized with TDI. The immunoreactivity of substance P (SP) and calcitonin gene-related peptide (CGRP) in the nerve terminals in the nasal mucosa was increased after intranasal application of TDI. We also observed a decrease in the immunoreactivity of SP and CGRP, and an increase in their mRNA expression in the trigeminal ganglion neurons. These findings indicate that exposure to TDI enhanced the biosynthesis of both SP and CGRP in the trigeminal ganglion neurons and their axonal transportation to the terminals in the nasal mucosa. In animals pretreated with capsaicin before sensitization, TDI did not induce nasal allergy-like behaviors and histamine release in the nasal mucosa. Since capsaicin depletes SP and CGRP in the sensory nerves, this finding indicates neuropeptide-mediated histamine release in the nasal mucosa. All these findings suggest that, on exposure to TDI, the antidromic release of SP and CGRP in the nasal mucosa triggers the release of histamine, resulting in the development of symptoms of nasal allergy.
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PMID:Neurogenic inflammation in nasal allergy: histochemical and pharmacological studies in guinea pigs. A review. 768 May 20

The effects of two tachykinin receptor antagonists, FK888 (selective antagonist at the tachykinin NK-1 receptor) and FK224 (dual antagonist at NK-1 and NK-2 tachykinin receptors), on the frequency of sneezing, decrease of nasal patency, and increase of vascular dye leakage induced by antigen challenge upon the guinea-pig nasal mucosa were studied. The animals were sensitized with ovalbumin intraperitoneally. FK224 inhibited and FK888 tended to inhibit the decrease of nasal patency induced by antigen challenge. The increase of vascular dye leakage from nasal mucosa induced by antigen challenge tended to be inhibited by both FK224 and FK888. But both of them did not inhibit the increase of sneezing induced by antigen challenge. We conclude that in the guinea-pig model of nasal allergy, tachykinin receptors mediate plasma leakage and swelling of nasal mucosa induced by antigen challenge, but the participation of an axonal reflex via tachykinin receptors is rather small compared to the direct vascular effect of chemical mediators.
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PMID:Effects of tachykinin receptor antagonists, FK224 and FK888, in a guinea-pig model of nasal allergy. 929 53


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