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)

Calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and substance P-like immunoreactivity (SP-LI) were evaluated in subnucleus caudalis following induction of sinusitis. Three days after induction, intensity of labeling for CGRP-LI and SP-LI increased in ipsilateral subnucleus caudalis. Labeling for CGRP-LI and SP-LI appeared normal at later time points (20 and 28 days). Early changes in these neuropeptides may contribute to the inflammatory process and painful symptoms accompanying sinusitis.
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PMID:Labeling of calcitonin gene-related peptide and substance P increases in subnucleus caudalis of rabbit during maxillary sinusitis. 959 42

Substance P (SP), one of the neuropeptides released from sensory nerves, is thought to mediate neurogenic inflammation. Although SP immunoreactive axons have been described in the sinus mucosa, no attempt has been made to characterize SP fibers as a subset of all axons present in the sinus mucosa. In addition, no study to date has characterized the changes in infected sinus mucosa. The maxillary sinus mucosa of New Zealand white rabbits was harvested from control animals and in animals with induced maxillary sinusitis. Immunohistochemical staining of the sinus mucosa for both Protein Gene Product 9.5 (PGP), a nonspecific marker for all nerves, and for SP was performed on 11 animals: 3 controls and 8 infected. In sinus mucosa from the control rabbits, <50% of all axons labeled by PGP were immunoreactive for SP. In infected mucosa, the absolute number of axons found by PGP staining decreased and nearly all of these remaining fibers were also immunoreactive for SP. We conclude that the phenotypical labeling of nerve fibers seen in normal mucosa is altered by bacterial-induced infection.
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PMID:Substance P immunoreactive sensory axons as a subset of the total axonal population in the maxillary sinus of the rabbit: a characterization of normal and infected mucosa. 1125 58

Nasal sensory nerve stimulation leads to sensations of pain and congestion and nociceptive nerve axon response-mediated release of substance P that stimulates glandular secretion as an immediate-acting protective mucosal defense. Recruited parasympathetic reflexes cause submucosal gland secretion via muscarinic M3 receptors. Parasympathetic reflexes, sneezing, and other avoidance behaviors rapidly clear the upper airway of offending agents while protecting the lower airways. Dysfunction contributes to allergic, infectious, and other nonallergic rhinitides and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, restoring nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies.
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PMID:Neurogenic mechanisms in rhinosinusitis. 1189 43

Stimulation of the nasal sensory nerves leads to sensations of pain and stuffiness. Type C nociceptive nerve releases neuropeptides including substance P and calcitonin gene related peptides that increase plasma extravasation and glandular secretion. This axonal response acts as an immediate protective mucosal defense mechanism. Recruited parasympathetic reflexes cause submucosal gland secretion via acetylcholine and muscarinic M(3) receptors. Itching, sneezing, and other avoidance behaviors rapidly clear the offending agents from the upper airways and protect the lower airways. Dysfunction of these nerves may contribute to allergic rhinitis, infectious rhinitis, nasal hyperresponsiveness, and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, and so restores nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies. Human axon responses differ from those in animals, an important distinction that limits extrapolation from other species.
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PMID:Upper airway neurogenic mechanisms. 1196 45