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)

N-methyl-D-aspartate (NMDA) is an agonist used to identify neuronal receptive sites for dicarboxylic amino acid neurotransmitters; NMDA receptors are implicated in neuronal damage of ischemic or hypoglycemic origin in newborns although involved mechanisms remain to be identified. In the present study, 31P magnetic resonance spectroscopy with fast (6/min) data acquisition was used in newborn rat brain slices to measure changes of intracellular phosphocreatine and nucleotide triphosphate levels following extracellular NMDA applications. The rapid exhaustion of phosphocreatine stores in 50% of the total population of brain cells was induced in all cases by application of NMDA (30-45 s, 25-100 mM). It was not reproduced by other excitatory agents: potassium ions (24.6 mM, 4 min), isobutylxanthine (1mM), muscarine (10 mM), serotonin (0.1 mM) or substance P (10 microM). Such an effect of NMDA was not modified after tetrodotoxin (1 microM) and was reduced by extracellular 2-amino-5-phosphonovalerate (50 microM) or magnesium ions (2.2 mM). However it did develop during NMDA-induce neuronal excitations and was reversible within 10-30 min. This action of NMDA was followed by an irreversible decrease of phosphorus metabolites if mitochondrial creatine kinase and adenosine triphosphatase were decoupled by atractyloside (50 microM). Experiments revealed a link between selective NMDA action at neuronal plasma membranes, neurotoxicity and energy production by mitochondria.
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PMID:Metabolic action of N-methyl-D-aspartate in newborn rat brain ex vivo: 31p magnetic resonance spectroscopy. 268 43

An intact nociceptor system of primary afferent sensory nerves is important for the initiation of the inflammatory process and successful tissue repair. Dysfunction of this system could be a contributing factor for delayed wound healing in humans. We examined the levels of vasodilators [substance P (SP), calcitonin gene-related peptide (CGRP)] and a vasoconstrictor peptide [neuropeptide Y (NPY)] in the peripheral blood samples of patients with burns covering from 20 to 75% of body surface area. Thirteen patient samples were obtained immediately on admission (OA), which was within 12 h of the thermal injury, and 24 h post-admission (PA). Enzyme immunoassay techniques were used for the measurement of the neuropeptides. In addition, an inflammatory marker, tumour necrosis factor-alpha (TNF-alpha), and a myofibrillar protein, creatine kinase (CK), were examined and compared with levels in 13 control subjects. CGRP was high OA and the levels were maintained PA (P < 0.05). SP was also significantly high at both sampling times (P < 0.05). Although TNF-alpha and NPY were somewhat higher in the patients' samples than in the control samples, these levels were not statistically significant (P = NS). CK was higher OA (P < 0.01) than PA (P < 0.04), compared to controls. Plasma levels of SP and CGRP increased significantly in patients with thermal injuries. These peptides may yet be another group of neuromodulators playing a significant role in immune, pain, inflammatory and wound healing in burns.
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PMID:Levels of vasodilators (SP, CGRP) and vasoconstrictor (NPY) peptides in early human burns. 1126 54

We previously found that the expression of transient receptor potential vanilloid 1 (TRPV1) and contents of calcitonin gene-related peptide (CGRP) and substance P (SP), two main neuropeptides released from TRPV1, were decreased in diabetic hearts. This study aimed to test whether decreased TRPV1, CGRP and SP levels were responsible for the loss of cardioprotection by ischemic postconditioning (IPostC) in isolated perfused heart from streptozotocin-induced diabetic rats. IPostC effectively protected non-diabetic hearts against ischemia/reperfusion injury by improving cardiac function and lowering creatine kinase (CK) and cardiac troponin I (cTnI) release, which could be abolished by inhibiting TRPV1, CGRP receptor or SP receptor. However, IPostC had no effect on cardiac function and the release of CK and cTnI in diabetic hearts regardless of whether TRPV1, CGRP receptor or SP receptor were inhibited. CGRP or SP-induced postconditioning significantly prevented both non-diabetic and diabetic hearts from ischemia/reperfusion injury by improving cardiac function and lowering CK and cTnI release. Additionally, IPostC markedly increased CGRP and SP release in non-diabetic hearts, which could be reversed with TRPV1 inhibition, but not CGRP receptor or SP receptor inhibition. However, IPostC failed to affect CGRP and SP release in diabetic hearts in the presence or absence of TRPV1, CGRP receptor or SP receptor inhibition. These results indicate that the loss of cardioprotection by IPostC during diabetes is partly associated with a failure to increase CGRP and SP release, likely due to decreased TRPV1 expression and CGRP and SP contents in diabetic hearts.
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PMID:Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P. 2155 4