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 is a decapeptide which forms part of the group known as neuropeptides, that is, peptides released by some neurones such as the slow-conducting C fibres and the rapid-conducting A-delta fibres. These neurones belong to the category of non-adrenergic non-cholinergic nerves (NANC), which perform their action through a mechanism known as "axonic reflex". This mechanism is an antidromic stimulation which produces a secretion of neuropeptides, especially substance P. It is known that substance P, once released, is able to exert a number of actions including among others inflammatory and bronchospastic activities and a stimulation of the immunologic system. Other effects attributed to this substance are an increase in capillary permeability and oedema and the perpetuation of certain conditions such as asthma, rhinitis and chronic urticaria or hives. The production, metabolism and actions of this neuropeptide are described.
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PMID:[Substance P: immuno-allergic implications]. 138 Jul 67

Angiotensin converting enzyme inhibitors (ACEI) are used widely in the treatment of both hypertension and congestive heart failure. Although usually well tolerated, these medications may produce side effects that may be encountered by the allergist, including cough, angioedema, and rhinitis symptoms. The severity of ACEI-induced cough may vary, and is associated with increased bronchial hyperreactivity in some (but not all) patients as judged by methacholine sensitivity. Angiotensin converting enzyme inhibitor-induced cough may have its onset from one day to 12 months after initiation of therapy, and is not dose dependent. Angioedema caused by ACEI is usually mild and clears with discontinuation of the drug, however cases requiring intubation and tracheostomy have been reported. The mechanism of ACEI-induced cough remains unclear, but could be in part due to accumulation of substances whose degradation may also be impeded by ACEI, such as substance P, bradykinins, and/or prostaglandins. Knowledge of the side effects produced by this class of medication may help patients avoid unnecessary, costly, and often invasive diagnostic evaluations.
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PMID:Angiotensin converting enzyme inhibitors and the allergist. 222 91

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

We compared the rise in nasal airway resistance (NAR) provoked by topical application of substance P (SP) and of methacholine (MCH) in seventeen patients suffering from rhinitis and fourteen control subjects. Challenges with SP or MCH were separated by a week or more. NAR was measured by posterior rhinomanometry before and 10 min after intranasal administration of SP (10-40 nmol) or MCH (3-12 mumol). The two groups of subjects had similar baseline levels of NAR and similar small responses to buffered saline. Substance P but not MCH provoked cutaneous flushing in all subjects. Both SP and MCH provoked a significantly greater increase in NAR in patients suffering from rhinitis than in control subjects. The increase in NAR was dose-dependent, and on a molar basis, SP was 375-500-fold more potent than MCH. Pretreatment with 200 micrograms of a topically active anticholinergic agent, oxytropium bromide, prevented the rise in NAR caused by 12 mumol of MCH but not that caused by 40 nmol of SP in six patients suffering from rhinitis. We conclude that SP is absorbed across the nasal mucosa and causes cutaneous vasodilation, that MCH and SP cause a greater rise in NAR in patients suffering from rhinitis than in control subjects, that SP is about 500-fold more potent than MCH in increasing NAR, and that the rise in NAR caused by SP is not mediated by postganglionic parasympathetic mechanisms.
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PMID:Nasal response to substance P and methacholine in subjects with and without allergic rhinitis. 245 27

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

Electrical stimulation of the maxillary branches of the trigeminal nerve induced an increase in vascular permeability to macromolecules and an interstitial edema in the nasal mucosa of the rat, as indicated by extravasation of Evans blue. In animals that had been treated neonatally with capsaicin, the effect of trigeminal nerve stimulation was abolished. Local application of capsaicin or substance P (SP) also induced a significant Evans blue extravasation in the nasal mucosa. In capsaicin-pretreated animals the effect of SP was still present, while the permeability increase induced by capsaicin was abolished. In conclusion, chemogenic irritation of the nasal mucosa by capsaicin induces edema probably via a local axon reflex inducing release of SP. Capsaicin-sensitive SP-containing afferents in the nasal mucosa may also be involved in the pathogenesis of nasal congestion seen in various types of rhinitis.
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PMID:Increased vascular permeability in rat nasal mucosa induced by substance P and stimulation of capsaicin-sensitive trigeminal neurons. 619 87

The functional effects of the intranasal application of exogenous vasoactive intestinal polypeptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) were evaluated in 12 healthy volunteers before and after neutral endopeptidase (NEP) inhibition with phosphoramidon (PA) and angiotensin-converting enzyme (ACE) inhibition with captopril. The three neuropeptides increased nasal airway resistance (NAR) measured by anterior rhinomanometry and superficial capillary blood flow measured by laser Doppler flowmetry (LDF). After pretreatment of the nasal mucosa with PA, the effects of VIP, SP and CGRP on the LDF signal, NAR and mucus production were potentiated, whereas local pretreatment with captopril did not modify these functional effects. These observations suggest that NEP, but not ACE, may participate in the catabolism of neuropeptides when applied directly to the human nasal mucosa. Furthermore, since these neuropeptides induced nasal obstruction, increased blood flow and rhinorrhea, a decreased activity of the enzymes involved in their degradation could be involved in the physiopathology of rhinitis symptoms.
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PMID:Functional effects of phosphoramidon and captopril on exogenous neuropeptides in human nasal mucosa. 754 Dec 10

Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome.
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PMID:RADS and RUDS--the toxic induction of asthma and rhinitis. 793 8

The morbidity of allergic airway disease and the number of deaths resulting from it have not declined in the past ten years. The multiplicity of mediators released in the acute allergic reaction and our limited knowledge of the basic mechanisms that drive chronic inflammation have hampered the design of effective therapeutic regimens for this type of disease. In this article, Claude Bertrand and Pierangelo Geppetti summarize recent studies in which new, potent and selective tachykinin and kinin receptor antagonists demonstrate the involvement of tachykinins and kinins in airway anaphylaxis, and review how these antagonists might be of use in treating allergic asthma and rhinitis.
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PMID:Tachykinin and kinin receptor antagonists: therapeutic perspectives in allergic airway disease. 875 84

Exogenous substance P (10-80 nmol/ml) induced a dose-dependent increase in nasal symptoms in asymptomatic allergics with rhinitis (n = 15) and controls (n = 8), but did not release any mediators. However, comparing the antigen-evoked release of mediators into nasal secretions with that of a substance P-pretreated antigen challenge, we found a significant enhancement of kinins, TAME esterase activity (p < 0.05-0.01), and histamine (p < 0.001, NS) 10-20 min after antigen challenge. These results suggest 1) that substance P-induced increase in nasal congestion is mediated through direct neurokinin receptor activation independently of mast cell activation, and 2) that during the allergic reaction there is a substance P-mast cell interaction that enhances the mediator response to nasal allergen challenge.
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PMID:Substance P enhances antigen-evoked mediator release from human nasal mucosa. 882 6


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