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

The purpose of the present study was to evaluate the modulatory effects of sensory neuropeptides on peripheral blood mononuclear leukocytes of normal and allergic subjects. Peripheral blood mononuclear leukocytes obtained from five normal subjects and from five patients with allergic rhinitis and asthma were incubated with morphine, ACTH, vasoactive intestinal peptide, or substance P at concentrations of 10(-9) M, 10(-7) M, 10(-6) M and suboptimal (0.0125 microgram/mL, 0.025 microgram/mL, and 0.05 microgram/mL) concentrations of PHA. Uptake of 3H-thymidine was evaluated at 72 hours of culture. An inhibitory effect was observed with morphine, ACTH, and substance P while stimulatory effects were seen with vasoactive intestinal peptide, both in normal and in allergic subjects. The results of these preliminary studies provide further evidence for a modulatory role of neuropeptides on the immune function in both normal and allergic subjects.
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PMID:In vitro studies of the modulatory effects of sensory neuropeptides on peripheral blood mononuclear leukocytes of normal and allergic subjects. 168 92

Responses to mite antigen and nonimmunological stimuli, substance P, of chopped fragments of nasal mucosae were studied from eleven patients with perennial allergic rhinitis who were sensitive to mite antigen. Amount of released histamine significantly increased by either stimulation. However, the release of leukotrienes (LTs) increased only by the stimulation of mite antigen, which correlated with that of histamine. By either stimulation, amount of histamine release tended to be higher in patients with severe nasal symptoms than in those with moderate nasal symptoms. Only by mite antigen stimulation, amount of the release of peptide LTs and LTB4 tended to be higher in patients with severe nasal symptoms. We concluded that the amounts of histamine and LTs released from nasal mucosa in allergic reaction were closely related with the severity of nasal symptoms in patients with allergic rhinitis.
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PMID:[A study of chemical mediators in patients with allergic rhinitis. 3). Release of histamine and leukotrienes from in vitro nasal mucosa]. 171 33

Our purpose was to characterize the tachykinin receptor type involved in nasal obstruction to exogenous substance P in rhinitic patients. We also attempted to assess biochemical and cellular events associated with this response. Nasal challenges were performed in seven patients with allergic rhinitis. They received increasing doses (10 to 80 nmol) of substance P, of neurokinin A, of the N-terminal fragment of substance P, substance P(1-9), and of saline on 4 different days separated by 14 days. Nasal airway resistance (NAR) increased in a dose-dependent manner on substance P. Maximal increase reached 4.5-fold basal NAR. Response to neurokinin A was significantly lower (less than 2-fold basal NAR). No effect was observed on substance P(1-9) and saline. This order of activity [substance P much greater than neurokinin A greater than substance P(1-9) = saline] indicates an NK1 receptor-mediated mechanism inducing local vasodilation. No histamine release was found after any of the four challenges. Proteins significantly increased in nasal lavage fluid on both substance P and neurokinin A, whereas substance P(1-9) and saline had no effect. The percentage of albumin increased in nasal lavage fluid from 30 to 50% of total proteins on substance P and neurokinin A, indicating microvascular leakage. Polymorphonuclear cells significantly increased from 9 to 36% on substance P, from 13 to 49% on neurokinin A, and from 13 to 55% on substance P(1-9). Eosinophils increased in five patients on substance P (from 0.1 to 5% for the group), in three patients after neurokinin A, and in two after substance P(1-9).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and inflammatory responses to exogenous tachykinins in allergic rhinitis. 171 29

The concentrations of the neuropeptides substance P, somatostatin, and calcitonin gene-related peptide in human nasal secretions were quantified by radioimmunoassays, concurrently with that of histamine, in the course of nasal challenge of allergic and control subjects with ryegrass antigen to examine contributions of neuromediation of the tissue response. Each of the neuropeptides and histamine were detected in nasal lavage fluid prior to challenge. In allergic patients, but not normal controls, antigen evoked significant increases of 3-fold in histamine at 15-60 min, 1.5- to 4-fold in calcitonin gene-related peptide at 15 min-24 hr, and more than 2-fold in somatostatin at 6 hr, without altering the concentration of substance P in nasal lavage fluid. The identity of the neuropeptides was confirmed chromatographically. Thus calcitonin gene-related peptide may mediate nasal congestion directly and somatostatin may be one of the factors regulating the late involvement of basophils and mast cells in allergic rhinitis.
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PMID:Distinctive patterns of release of neuroendocrine peptides after nasal challenge of allergic subjects with ryegrass antigen. 245 30

We have studied the changes in concentration of serotonin, substance P, and vasoactive intestinal peptide (VIP) in plasma following a nasal allergen provocation in 14 grass pollen-allergic subjects; in five the urinary excretion of serotonin and 5-hydroxy-indolyl-acetic acid (5-HIAA) was also measured. In addition, the concentration of serotonin and substance P was measured in nasal secretions following nasal challenge with allergen and methacholine. The results showed an allergen-induced increase in free plasma serotonin (P less than 0.01) and no change in platelet serotonin, urinary serotonin and urinary 5-HIAA. The plasma substance P level tended to fall (P greater than 0.1), while plasma VIP increased significantly (P less than 0.02). In nasal secretions, there were measurable levels of serotonin in all samples and of substance P in all but one. There was no difference between the concentrations of serotonin and substance P in secretions collected after allergen challenge and after methacholine challenge. For both substances, the secretion median value was comparable to that of plasma. Symptom reduction by topical and systemic pretreatment with a serotonin- and VIP-antagonist before nasal allergen provocation is necessary to define the role of these two agents in allergic rhinitis.
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PMID:Effect of nasal allergen challenge on serotonin, substance P and vasoactive intestinal peptide in plasma and nasal secretions. 245 56

Nasal challenge and intradermal injection with substance P (SP) were performed in five normal subjects and in five patients suffering from allergic rhinitis. No clinical symptoms, local histamine release, or modifications of nasal airway resistance were observed when SP was insufflated in the nose. Conversely, intradermal injection with SP caused a wheal and flare reaction in all the studied subjects. The different response to SP is likely to be due to the heterogeneity of human skin and nasal mucosa mast cells as far as sensitivity to histamine-releasing agents is concerned. Our findings indicate that SP has no relevant effect on human nasal mucosa, even if a synergetic action of SP with other allergic mediators cannot be excluded. The role of SP in the pathogenesis of allergic diseases in humans remains to be defined and deserves further study.
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PMID:Activity of substance P on human skin and nasal airways. 245 61

We studied the role of neutral endopeptidase (NEP) and kininase II (angiotensin-converting enzyme; ACE) in the modulation of exogenous substance P (SP)-induced nasal response in normal subjects and in patients with allergic rhinitis. We measured the nasal conductance in response to increasing doses of SP 2 h after oral administration of either placebo or the ACE inhibitor, cilazapril (5 mg), or the NEP inhibitor, acetorphan (300 mg), given in a randomized, double-blind, cross-over manner. We performed three separate studies: acetorphan versus placebo and cilazapril versus placebo, in normal subjects (n = 6 and n = 8, respectively), and acetorphan versus cilazapril versus placebo in patients with allergic rhinitis (n = 6). In normal as well as in rhinitic subjects, SP decreased nasal conductance in a dose-dependent fashion (p < 0.001). With placebo, the decrease in nasal conductance in normal subjects was similar to that in patients with allergic rhinitis (p > 0.5). In normal subjects, acetorphan potentiated the decrease in nasal conductance (p < 0.001), whereas cilazapril did not (p = 0.12). In patients with allergic rhinitis, the decrease in nasal conductance was potentiated by acetorphan (p < 0.001) and by cilazapril (p < 0.001). With acetorphan, the decrease in nasal conductance was not different in patients with allergic rhinitis and in normal subjects (p > 0.9). Conversely, with cilazapril, the nasal response to SP was greater in patients with allergic rhinitis than in normal subjects (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of neutral endopeptidase and kininase II on substance P-induced increase in nasal obstruction in patients with allergic rhinitis. 750 44

In the last decade, several neuropeptides have been localized in sensory, sympathetic and parasympathetic neurons of the upper and lower airways in animals and man. Tachykinins are sensory neuropeptides: after nasal allergen challenge in patients with allergic rhinitis, substance P is locally released and induces nasal obstruction. Like neurokinin A, another tachykinin of sensory C fibers, substance P induces an increase in vascular permeability and a recruitment of inflammatory cells. Thus, tachykinins partially mimic nasal response to antigen. Calcitonin gene-related peptide (CGRP) is another sensory neuropeptide and vasoactive intestinal peptide (VIP) is a neuropeptide localized to parasympathetic fibers. The distributions of CGRP and VIP fibers and of their binding sites, as well as their physiological effects described in other tissues, are consistent with a vasodilator effect. On the other hand, neuropeptide Y (NPY), a sympathetic neuropeptide, would seem to be a potent vasoconstrictor. Thus, nasal neuropeptides, and above all sensory neuropeptides, could play a role in the pathophysiology of allergic rhinitis.
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PMID:[Neuropeptides of the nasal innervation and allergic rhinitis]. 752 27

The effects of nasal administration of increasing doses of exogenous substance P have been studied in patients with allergic rhinitis treated with placebo or with the H1 antagonist cetirizine (10 mg twice daily for 3 days). Responses to substance P were assessed by posterior rhinomanometry (measuring nasal airway resistance) and by measure of histamine, protein and albumin production and cell recovery in nasal lavage fluids before and after challenge. Substance P induced a dose-dependent increase in nasal airway resistance which was similar after treatment with either cetirizine or placebo (maximal increase in nasal airway resistance was 4.2-fold greater than the baseline with the placebo and 4.7-fold greater than the baseline with cetirizine). No histamine release was observed. Similar increases in protein and albumin production were observed after stimulation with substance P along with the placebo (protein: from 0.35 +/- 0.11 to 3.31 +/- 0.62 mg and albumin: from 0.09 +/- 0.04 to 2.08 +/- 0.39 mg) and when combined with cetirizine treatment (proteins: from 0.42 +/- 0.09 to 3.62 +/- 0.77 and albumin: from 0.17 +/- 0.04 to 2.19 +/- 0.51 mg). After stimulation with substance P, percentages of neutrophils recovered in nasal fluids increased from 26.2 +/- 11.5 to 54.5 +/- 9.5 with the placebo and from 35.5 +/- 11.0 to 53.6 +/- 9.5 with cetirizine. Eosinophils were inconsistently found after substance P stimulation during both treatments. In conclusion, nasal response to substance P is not modified by cetirizine which suggests that the effect of substance P is not secondary to histamine release in the nose in man.
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PMID:Do nasal mast cells release histamine on stimulation with substance P in allergic rhinitis? 784 59


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