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 (SP) and vasoactive intestinal peptide (VIP) concentrations in nasal secretions and plasma from patients with nasal allergy to Japanese cedar pollen and healthy volunteers were measured from Jan to Dec, 1991 using EIA established by us. Simultaneously, the numbers of airborne pollens of Japanese cedar and cypress were counted, and the relation to the SP and VIP concentrations in nasal secretions from the patients with nasal allergy to Japanese cedar pollen was studied. The mean SP concentration in nasal secretions from the patients with nasal allergy to Japanese cedar pollen in the pollination season was 81.9 +/- 48.4 fmol/mg protein, which was significantly higher than that in the non-pollination season (30.4 +/- 14.7 fmol/mg protein) (p < 0.01). Likewise, the mean VIP concentration in nasal secretions from the patients with nasal allergy to Japanese cedar pollen in the pollination season was 14.2 +/- 10.4 fmol/ml protein, which was significantly higher than that in the non-pollination season (4.2 +/- 3.0 fmol/mg protein) (p < 0.01). The SP and VIP concentrations in nasal secretions from the healthy volunteers were not affected by the scattering of pollens. The SP and VIP concentrations in plasma from the patients and the healthy volunteers were not affected by the scattering of pollens.
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PMID:[Seasonal fluctuations of substance P and vasoactive intestinal peptide concentrations in nasal secretions of patients with nasal allergy to Japanese cedar pollen]. 128 39

Toluene diisocyanate (TDI) induces respiratory allergy in mammals. Using immunohistochemistry and in situ hybridization histochemistry, the present study examined effects of nasal mucosa sensitization by TDI on the immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) and on the expression of their mRNAs in guinea pig trigeminal ganglion and their terminals. Single intranasal application of TDI (acute experiment) did not induce nasal allergy-like behaviours and failed to cause changes of SP and CGRP immunoreactivity and in the expression of preprotachykinin A (PPTA) mRNA and preproCGRP mRNA coding for SP and CGRP respectively in the trigeminal ganglion neurons. However, repeated application of TDI (chronic experiment) caused a dramatic increase of SP and CGRP immunoreactivity in peripheral neurites of sensory nerves in the nasal mucosa but a slight increase in the spinal trigeminal nucleus, a decrease of the same immunoreactivities in the cell bodies of the trigeminal ganglion neurons, and an increase of the expression of PPTA and preproCGRP mRNA in the same neurons. These findings suggest that chronic exposure of the nasal mucosa to TDI apparently causes enhancement of both the biosynthesis of SP and CGRP and their axonal transport in the trigeminal system.
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PMID:Nasal mucosa sensitization with toluene diisocyanate (TDI) increases preprotachykinin A (PPTA) and preproCGRP mRNAs in guinea pig trigeminal ganglion neurons. 132 40

The sources of different chemical substances in the NF of allergic patient, such as albumin, secretory IgA, histamine, leukotriene, kinin and substance P were investigated. To accomplish this, we challenged the inferior turbinate on one side, but separately collected NF from both sides in patients with nasal allergy to house-dust. Provocation was done with paper disc containing dried allergen extract. Collection was done by suction for the first five minutes immediately after the onset of a positive response to nasal provocation. The total amount of the chemical substances on each side was analyzed separately and compared. Significant differences were seen between both sides only for histamine and leukotriene. In consideration with the previous reports, it is suggested that in nasal allergen challenge the major sources are glandular secretion for secretory IgA, and albumin, and secretion for migrating cells for histamine and leukotriene. The major sources responsible for kinin and substance P, however, are not defined.
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PMID:The sources of chemical substances in allergic nasal fluid. 171 74

Before terfenadine treatment, the mean substance P and vasoactive intestinal polypeptide (VIP) concentrations in nasal secretions from nasal allergy patients tended to be higher than the values of healthy subjects. During terfenadine treatment, the mean substance P concentrations in nasal secretions from patients allergic to house dust or pollen were significantly decreased to 62 and 39% of the initial values, respectively. The mean VIP concentrations in nasal secretions from the house dust allergy patients and the pollen allergy patients were significantly decreased to 52 and 18% of the initial values, respectively. Plasma substance P and VIP concentrations were not affected by nasal allergic symptom and terfenadine treatment.
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PMID:Effect of terfenadine on substance P and vasoactive intestinal polypeptide concentrations in nasal secretions from patients with nasal allergy. 751 18

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

To clarify the role of substance P (SP) and vasoactive intestinal peptide (VIP) in nasal allergy, we measured their concentrations in the nasal secretions and plasma of normal subjects and patients with nasal allergy to house dust and Japanese cedar pollen by competitive enzyme-linked immunoassay. The mean levels of SP (224 pmol/L) and VIP (41.6 pmol/L) in the nasal secretions of normal subjects were significantly higher than those in plasma (SP 3.04 pmol/L and VIP 1.04 pmol/L; p < .01). The mean levels of SP and VIP in the nasal secretions of the pollinosis group were significantly higher than those of the control group (p < .05 and p < .01), while the levels of the house dust allergy group were not higher than those of the control group. Intranasal allergen challenge significantly reduced SP levels in the nasal secretions of the allergy groups, while it did not influence VIP levels in the nasal secretions. These findings suggest that SP and VIP are actively secreted into the nose and may play an important role in the allergic reaction on the surface of the human nasal mucosa.
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PMID:Substance P and vasoactive intestinal peptide in nasal secretions and plasma from patients with nasal allergy. 767 75

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 topically administered substance P (SP) on nasal blood flow and nasal airway resistance (NAR) were evaluated in 11 subjects with perennial nasal allergy. The change in NAR induced by SP was compared with those induced by nasal challenge with histamine, leukotriene D4 (LTD4), and antigen. In doses > or = 16 nmol, SP caused a significant increase of nasal blood flow within 5 minutes that lasted for less than 20 minutes. In doses > or = 16 nmol, SP caused a dose-dependent, short-lasting, significant increase in NAR. The magnitude of the increase in NAR was LTD4 > SP > histamine when compared on a molar basis. Our results may suggest that SP released from C fiber terminals is partially involved in an early nasal vascular response after antigen challenge by acting on adjacent vascular smooth muscle to cause a transient vasodilatation of both resistance and capacitance vessels only while sensory stimulation persists in subjects with nasal allergy.
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PMID:Role of substance P in the vascular response of nasal mucosa in nasal allergy. 871 37

To clarify the effects of anti-allergic drugs on substance P (SP) and vasoactive intestinal peptide (VIP) levels in nasal secretions, we employed competitive enzyme-linked immunoassays to measure concentrations of those neuropeptides in nasal secretions from 40 patients with house dust nasal allergy before and after administration of azelastine and oxatomide. One mg of azelastine and 30 mg of oxatomide were administrated twice a day for 4 weeks. Mean values of SP concentrations and ratios of SP to total protein of the nasal allergy group were significantly higher than those of the control group (p < 0.002). The VIP/total protein ratio of the allergy group was also significantly higher than that of the control group, although the VIP concentration alone was not. Mean levels of SP and VIP from patients with severe symptoms were significantly higher than those of the control group (p < 0.05), although those values were not significantly different between patients with moderate symptoms and control subjects. Azelastine and oxatomide effectively reduced SP levels in nasal secretions (p < 0.005), but they did not significantly decrease VIP levels. The reduction of SP levels was significant in patients with excellent responses to those drugs (p < 0.005), but not in patients with poor responses. These findings suggest that SP and VIP levels in nasal secretions may reflect the clinical state of nasal allergy and be one of the better parameters available for evaluating the clinical efficacy of anti-allergic drugs against nasal allergy.
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PMID:Effects of anti-allergic drugs on substance P (SP) and vasoactive intestinal peptide (VIP) in nasal secretions. 920 98

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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