Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

1. Substance P (SP) induces histamine release from isolated rat peritoneal mast cells at concentrations of 0.1-10 muM.2. Inhibitors of glycolysis and oxidative phosphorylation prevent the release of histamine induced by SP.3. Cells heated to 47 degrees C for 20 min release histamine when treated with an agent causing cell lysis but fail to release in response to SP.4. SP does not release histamine by interacting with cell-bound IgE.5. Histamine release by SP is rapid, with more than 90% of the response occurring within 1 min of the addition of the peptide to mast cells at 37 degrees C.6. Substance P, unlike antigen-antibody or compound 48/80, does not show enhanced release of histamine when calcium (0.1-1 mM) is present in the extracellular medium but calcium increases the response to SP when the ion is added after the peptide. Extracellular calcium (0.1-1 mM), magnesium (1-10 mM) and cobalt (0.01-0.1 mM) all inhibit SP-induced histamine release when added before the peptide. Pre-treatment of the cells with EDTA (10 mM) and washing in calcium-free medium inhibits the histamine release induced by SP.7. Histamine release induced by SP was optimum at an extracellular pH of 7.2.8. A number of peptides structurally related to SP were examined for histamine-releasing activity. At the concentrations tested, the N-terminal dipeptides Lys-Pro and Arg-Pro, tuftsin, physalaemin, eledoisin, SP(3-11), SP(4-11) and [p-Glu(6), p-amino Phe(7)]-SP(6-11) were all found to be inactive. The relative activities of the other peptides were: [Formula: see text]9. Rat basophilic leukaemia cells (RBL-2H3) fail to respond to SP at concentrations which activate rat mast cells. Release of 5-hydroxytryptamine by immunological activation of RBL cells is not changed by the presence of SP.10. The mechanism of action of SP on mast cells and the nature of the SP receptor on mast cells is discussed in relation to SP receptors in other cell types.
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PMID:The effects of substance P on histamine and 5-hydroxytryptamine release in the rat. 618 68

Electrical stimulation of the cervical vagus nerve in anesthetized guinea pigs induced a rapid increase in respiratory insufflation pressure, suggesting increased airway resistance. After intravenous administration of a substance P (SP) antagonist, [D-Arg(1),D-Pro(2),D-Trp(7,9),Leu(11)]SP, the insufflation pressure response to vagal stimulation was reduced by 78% while the cardiovascular effects were unchanged. Histamine receptor-blocking agents were used to inhibit the effects of histamine release induced by the SP-antagonist. [D-Arg(1),D-Pro(2),D-Trp(7,9),Leu(11)]SP also reduced the increase in insufflation pressure caused by intravenous SP or capsaicin. The long-lasting noncholinergic contraction of the main and hilus bronchi induced by field stimulation in vitro, as well as the contractile effects of SP and capsaicin, were also blocked by the SP antagonist. The cholinergic contractions and the noncholinergic tracheal relaxation on field stimulation in vitro were, however, not blocked by the antagonist. Vagal stimulation in vivo also increased vascular permeability in the respiratory tract and esophagus, causing a subepithelial edema as indicated by Evans blue extravasation. Previous treatment with [D-Arg(1),D-Pro(2),D-Trp(7,9),Leu(11)]SP inhibited the permeability increase induced by both vagus nerve stimulation and exogenous SP. SP release from vagal sensory nerves was indirectly shown by reduction in the bronchial levels of SP after nerve stimulation in vivo. The data suggest that a major portion of the vagally or capsaicin-induced increase in smooth muscle tone is caused by SP release from sensory neurons. In addition, activation of vagal SP-containing sensory nerves induces local edema. Tracheobronchial afferent SP-containing C fibers may thus exert local control of smooth muscle tone and vascular permeability in normal and pathophysiological conditions.
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PMID:A substance P antagonist inhibits vagally induced increase in vascular permeability and bronchial smooth muscle contraction in the guinea pig. 618 20

Anterolateral deafferentation of the rat medial basal hypothalamus was used to eliminate most of the somatostatinergic innervation of the stalk-median eminence while leaving a functional system producing GH-releasing factor (GHRF) in the partially deafferented hypothalamus. One week after the operation, the rats were anesthetized, the third ventricle was cannulated, and various putative neurotransmitters were infused for 5 min. Plasma GH levels were measured between 10 and 25 min after infusion. When infused into the third ventricle, acetylcholine (50 micrograms), substance P (5 micrograms), dopamine (5 micrograms), and norepinephrine (2.5 micrograms) increased plasma GH levels in the deafferented rats but not in the controls, while 5-hydroxytryptamine (5 micrograms) caused a rise of plasma GH levels in both groups. Histamine (5 micrograms) failed to alter GH in any of the groups. We suggest that acetylcholine, substance P, norepinephrine and dopamine, but not histamine, may increase the secretion of GHRF acting either directly upon the GHRF cells or on neural circuits impinging upon them.
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PMID:Various putative neurotransmitters affect growth hormone (GH) release in rats with anterolateral hypothalamic deafferentation of the medial basal hypothalamus: evidence for mediation by a GH-releasing factor. 619 Jun 42

Histamine secretion was induced by substance P, in a dose-dependent manner, from rat peritoneal mast cells, both in the presence and absence of Ca2+ in the medium, and disodium cromoglycate (DSCG) produced a dose-dependent inhibition of the histamine secretion in Ca2+-containing medium. However, in the absence of Ca2+, DSCG was ineffective or had a far weaker activity. Mg2+, Sr2+ and Ba2+ were ineffective in restoring the DSCG activity when added to medium devoid of divalent metal ions. Therefore, extracellular Ca2+ seems to be a specific requirement for the binding of DSCG to its "receptors" on the mast cell surface or some steps in the DSCG action.
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PMID:Disodium cromoglycate inhibition of substance P-induced histamine secretion is calcium dependent. 619 41

The effects of the substance P analogue (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP on the ocular inflammatory responses (miosis, vasodilation, protein leakage into the aqueous humour and eye pressure rise) to antidromic trigeminal nerve stimulation (trigeminal stimulation), intracameral injections of substance P (SP), capsaicin, prostaglandin E1 (PGE1), compound 48/80 and histamine were investigated in albino rabbits. The effects of nerve blockade with tetrodotoxin and blockade of histamine receptors on the responses to compound 48/80 and histamine were also investigated. Histamine H1 receptors were blocked with clemastin and H2 receptors with cimetidin. Formation of endogenous prostaglandins was prevented with indomethacin. The pupil size and the eye pressure were measured. The aqueous humour was collected immediately after the animal was killed, and analyzed for protein concentration. (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP had no significant miotic effect, but tended to cause a break-down of the blood-aqueous barrier. Miosis caused by SP, trigeminal stimulation, capsaicin, PGE1, compound 48/80 or histamine was blocked by (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP. Histamine miosis was significantly reduced by blockade of nerve conduction or histamine receptors, while miosis caused by compound 48/80 was not. Nerve blockade abolished the rise in intraocular pressure caused by compound 48/80. Our results indicate that (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP is a specific SP blocker in the sphincter pupillae muscle. They are strong evidence for the hypothesis that trigeminal stimulation and capsaicin cause miosis by release of SP or a related substance (SPLI), and it seems likely that the miosis caused by PGE1 and compound 48/80 is also caused by SPLI release. Histamine miosis is probably mediated both by SP receptors and histamine receptors in the pupillary sphincter muscle.
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PMID:Effects of the substance P antagonist, (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP on the miotic response to substance P, antidromic trigeminal nerve stimulation, capsaicin, prostaglandin E1, compound 48/80 and histamine. 620 97

Norathyriol, a xanthone aglycon isolated from Tripterospermum lanceolatum, was demonstrated to reduce the plasma leakage elicited by the passive cutaneous anaphylactic reaction in normal as well as in adrenalectomized mice. Capsaicin pretreatment greatly suppressed the local edema caused by antidromic stimulation of the saphenous nerve. The plasma exudation of neurogenic inflammation was also reduced in mice treated with norathyriol, diphenhydramine and methysergide, but not with indomethacin. Norathyriol, cyproheptadine and diphenhydramine combined with methysergide suppressed the ear edema caused by injection of compound 48/80, bradykinin and substance P into the ear. However, indomethacin did not affect this phlogist-induced edema response. Histamine- and serotonin-induced plasma exudation in ear edema was also reduced by norathyriol. In isolated rat peritoneal mast cell preparations, norathyriol produced a dose-dependent inhibition of histamine and beta-glucuronidase release from mast cells challenged by compound 48/80, bradykinin and substance P. In compound 48/80-pretreated mice, norathyriol at higher concentrations suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine combined with methysergide did. These data indicate that the inhibitory effect of norathyriol on local edema is not due to the release of steroid hormones from the adrenal gland, but is probably partly due to suppression of mast cell degranulation and hence reduce the release of chemical mediators which increase vascular permeability, and partly, at least in higher doses, due to protection of the vasculature from challenge by various mediators.
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PMID:Inhibitory effect of norathyriol, a xanthone from Tripterospermum lanceolatum, on cutaneous plasma extravasation. 751 Nov 7

Recent evidence suggests that the level of interleukin-6 (IL-6) is elevated in Alzheimer's disease (AD) brains. IL-6 is produced by reactive glial cells and could potentially affect neuronal survival. Understanding the biochemical mechanism that regulates the production and release of IL-6 by astrocytic cells may help to identify potential targets for therapeutic intervention in AD. In the present study, glial fibrillary acidic protein-positive human U373MG astrocytoma cells were used as a model of reactive astrocytes. Production of IL-6 in response to drug treatment was monitored with an ELISA assay. Histamine (1-100 microM), substance P (SP; 1-100 nM), and human interleukin-1 beta (IL-1 beta; 1-30 pM) stimulated the release of IL-6 in a time- and concentration-dependent manner, with EC50 values of 4.5 microM, 8 nM, and 4.5 pM, respectively. The respective effects of histamine, SP, and IL-1 beta were effectively blocked by the histamine H1, SP, and IL-1 receptor antagonists, supporting a receptor-mediated event for these agents. Both histamine and SP enhanced the formation of inositol phosphates and increase intracellular calcium levels, suggesting that the phosphatidylinositol bisphosphate/protein kinase C pathway may be involved in the IL-6 release process. Indeed, phorbol 12-myristate 13-acetate, a protein kinase C activator, also evoked IL-6 release from the U373MG cells. On the other hand, IL-1 beta, which produces a much more robust release of IL-6 than histamine or SP, has no effect on inositol phosphate formation or intracellular calcium levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the release of interleukin-6 from human astrocytoma cells. 751 68

Pilocarpine releases histamine from mast cells of cat submandibular gland and rat liver. In the salivary gland, histamine is released into the saliva and venous outflow. Atropine blocks the salivation, but not histamine release from the submandibular gland into the blood. Histamine release from the gland could be due to a direct action of pilocarpine on tissue mast cells or to an indirect action of mediators (acetylcholine and peptides). These hypotheses were further investigated in our present studies on rat peritoneal mast cells. Our results show: (1) histamine release from rat peritoneal mast cells induced by pilocarpine (ED50 = 1.7 x 10(-2) mol/l) occurs at 1000-fold higher concentrations than by substance P (ED50 = 1.7 x 10(-5) mol/l) and in 6.5-fold higher concentrations than by atropine (ED50 = 2.6 x 10(-3) mol/l), (2) pilocarpine injected directly into the rat peritoneal cavity causes histamine release from peritoneal mast cells in 1.8-fold higher concentrations than from isolated rat peritoneal mast cells. These results would support the hypothesis that histamine release from cat submandibular gland is caused by peptidergic co-transmission during the stimulation of the organ.
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PMID:The mechanism of histamine release induced by pilocarpine from different tissues: studies on rat peritoneal mast cells. 752 51

Histamine, acting via H1 receptors, dose-dependently stimulated [3H]inositol phosphate production in GT1-7 neuronal cells. GT1-7 cells also responded to Substance P but not to other neuroactive drugs tested. Acute histamine pretreatment desensitised the histamine-induced response, resulting in a reduction in the maximal response and a slower time-course of [3H]-inositol phosphate production. The desensitisation phenomenon was reversible, with full recovery by 2 h.
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PMID:An immortalised murine hypothalamic neuronal cell, GT1-7, expresses functional histamine H1 receptors. 752 86

Polymyxin B-induced hind-paw edema was suppressed by abruquinone A, an isoflavanquinone isolated from Abrus precatorius, in normal as well in adrenalectomized mice. Unlike dexamethasone, abruquinone A did not increase the liver glycogen content in fasting adrenalectomized mice. The volume of exuded plasma was significantly reduced by abruquinone A in neurogenic inflammation, passive cutaneous anaphylactic reaction and compound 48/80-induced ear edema. Histamine-, serotonin-, bradykinin- and substance P-induced plasma extravasation in ear edema was also suppressed by abruquinone A. Abruquinone A, like isoproterenol, significantly reduced the bradykinin- and substance P-induced plasma extravasation in normal as well as in compound 48/80-pretreated mice. In addition, abruquinone A suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine/methysergide did. In the in vitro experiments, abruquinone A suppressed the compound 48/80-induced histamine and beta-glucuronidase released from isolated rat peritoneal mast cell preparations. These results suggest that the anti-inflammatory effect of abruquinone A is mediated partly via the suppression of the release of chemical mediators from mast cells and partly via the prevention of vascular permeability changes caused by mediators. The glucocorticoid activity and the release of glucocorticoid hormones from the adrenal gland are probably not involved.
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PMID:Inhibition of plasma extravasation by abruquinone A, a natural isoflavanquinone isolated from Abrus precatorius. 753 81


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