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, present in primary sensory neurones, seems to take part in nociceptive transmission within the trigeminal system. Substance P, released by peripheral axons of these neurones, induces vasodilatation, plasma extravasation, miosis, conjunctival and nasal congestion. All these effects bear some similarity to symptoms of cluster headache and migraine attack. Opiates and somatostatin inhibit the release of substance P from primary sensory neurones and relieve both pain and autonomic symptoms of cluster headache attack. Plasma substance P-like immunoreactivity was decreased during spontaneous attack of cluster headache and migraine and during histamine precipitated attack of cluster headache. Taken together these data suggest that substance P and endogenous opioids could be implicated in the pathophysiology of cluster headache and migraine.
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PMID:Substance P and enkephalins: a creditable tandem in the pathophysiology of cluster headache and migraine. 243 12

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

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 article briefly describe the innervation of the human cerebral circulation by nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP). The neuropeptides in human cerebral arteries were characterized by radioimmunoassay in combination with HPLC. These neuropeptides mediate contraction (NPY) and dilation (VIP, SP, CGRP). In conjunction with spontaneous attacks of migraine or cluster headache, release of CGRP is seen. With the associated symptoms of nasal congestion and rhinorrhea, VIP is released. Successful treatment may abort the peptide release in parallel with disappearance of headache.
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PMID:Neuropeptides in the cerebral circulation: relevance to headache. 758 22

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

Rhinitis is defined as inflammation of the lining of the nose, characterized by one or more of the following symptoms: nasal congestion, rhinorrhea, sneezing and itching. Modifications of nose secretion and of the blood supply of the nasal mucosa are responsible for development of rhinitis. Cholinergic and adrenergic agents as well as histamine, 5-hydroxytriptamine, kallidin and substance P are mediators of inflammation in rhinitis. The topical pharmacological principles we have today for management of rhinitis include: antihistamines, corticosteroids, anticholinergic agents, decongestants, sodium cromoglycate, nasal douching and aromatic inhalations.
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PMID:[Topical treatment of rhinitis: current status. Physiopathologic and pharmacologic bases]. 1136 Aug 18

The sensory innervation of intracranial vessels originate in the trigeminal ganglion and comprise the following signal substances; calcitonin gene-related peptide (CGRP), substance P, neurokinin A, pituitary adenylate cyclase activating peptide (PACAP) and nitric oxide (NO). Studies in patients have revealed a clear association between head pain and the release of CGRP. In cluster headache and in a case of chronic paroxysmal headache there is in addition release of vasoactive intestinal peptide (VIP), which was associated with the facial symptoms (nasal congestion, rhinorrhea). In parallel with triptan administration, acting via 5-HT(1B/1D) receptors, head pain subside and neuropeptide release normalise. These data show the involvement of sensory and parasympathetic mechanisms in the pathophysiology of primary headaches.
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PMID:Sensory nerves in man and their role in primary headaches. 1159 8

The tachykinins, substance P (SP) and neurokinin A (NK-A), are thought to be key players in the process of neurogenic inflammation, which is believed to contribute to the pathogenesis of various respiratory diseases. Due to the additive nature of the respiratory effects of these sensory neuropeptides, inhibiting the effects of tachykinins at both NK1 and NK2 receptors may represent a therapeutic advantage for the treatment of asthma, as opposed to receptor-selective antagonists, which have demonstrated only minimal efficacy to date. A number of companies are pursuing small molecule approaches yielding compounds with potent, balanced NK1 and NK2 receptor antagonist activities. In allergic rhinitis, NK1 receptor antagonism may complement the actions of antihistamines by addressing nasal congestion, which is largely unrelieved by these otherwise highly efficacious agents. Novel combined H1/NK1 receptor antagonists have been developed and may represent a therapeutic option for the treatment of this disease.
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PMID:Combined tachykinin receptor antagonists for the treatment of respiratory diseases. 1599 15

Allergic rhinitis (AR) is a common airway disease characterized by mucosal swelling leading to congestion, mucosal hyperreactivity and increased secretions. Inflammatory processes in the mucosa are responsible for most symptoms and are characterized by mucosal remodeling after longer time periods. The early phase response, which is characterized by sneezing, rhinorrhea and nasal congestion, is the response of the sensory nerve terminals and blood vessels in the nasal mucosa to chemical mediators such as histamine, prostaglandins and leukotrienes. Nasal exposure to allergens leads to infiltration of inflammatory cells, such as activated eosinophils and T helper type 2 (TH2) cells, into the nasal mucosa by chemoattractant factors such as cytokines including interleukin 5 (IL-5), chemical mediators including cysLTs and chemokines including eotaxin. Edema of the nasal mucosa develops as a secondary reaction with inflammatory cells. This inflammation, referred to as the late-phase response, develops 6-10 h after allergen challenge and causes prolonged nasal congestion. In addition, a neurogenic mechanism is activated after liberation of substance P and others. Therefore, allergic rhinitis is a complex immunogenic disease that also activates mechanisms of the immune system in general. Antiallergic and antiinflammatory medications such as nasal glucocorticosteroids (nGCS) are thought to be the most effective treatment for controlling the symptoms and inflammatory mechanisms of AR. The antiinflammatory action of nGCS depends on at least two different mechanisms: transactivation and transrepression. Moreover, they regulate immune functions by inducing regulatory cytokines and forkhead box P3 (Foxp3). Foxp3 is of upmost importance as a transcription factor of regulatory t-cells, allowing the inhibition of effector function and proliferation of other CD4+ cells.
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PMID:[Mechanism of action of nasal glucocorticosteroids in the treatment of allergic rhinitis. Part 1: Pathophysiology, molecular basis]. 2253 81