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)

Polyphloretin phosphate (PPP) produced a dose-dependent decrease in the tone and reduction of the spontaneous phasic contactions of the longitudinal muscle of guinea-pig isolated ileum. PPP (100 microgram ml-1) after a 2 min contact with the ileum decreased the contractile effects of PGE1 0.1 micron by 40.6 +/- 7.4%, of PGE1 0.01 micron by 86.7 +/- 3.3% and of PGE2alpha 0.1 micron by 62.2 +/- 8.6%. After 10 min contact of PPP the contractile effect of PGE1 0.1 micron was decreased by 47.7 +/- 4.7% and that of PGE2alpha 0.1 micron by 89.6 +/- 1.7%. When the contact was longer, PPP showed a pronounced after-effect in respect to the effects of PGE1 and particularly of PGF2alpha. PPP signicantly reduced contractions to 5-HT and BaCL2, but not to acetylcholine, histamine or substance P. The type of antagonism of PGE1 by PPP was examined using cumulative concentration-effect curves for PGE1 in the presence of increasing concentrations of PPP. We conclude that on guinea-pig ileum PPP acts as a non-competitive antagonist of PGE1 and PGF2alpha.
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PMID:The character of the antagonism by polyphloretin phosphate of contractions to prostaglandins E1 and F 2alpha in guinea-pig ileum. 2 96

The effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HY-CRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0.0165 HE/ml and 0.5 HE/ml. Relative high doses of lysine-vasopressin showed a slight additive effect on the release of ACTH induced by 0.1 HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrotropin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, beta-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and gamma-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
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PMID:ACTH release in pituitary cell cultures. Effect of neurogenic peptides and neurotransmitter substances on ACTH release induced by hypothalamic corticotropin releasing factor (CRF). 3 43

Substance P has recently been localized in sensory nerves and has been suggested to be the mediator of antidromic vasodilatation. Interactions of substance P with putative mediators of inflammation and adenosine 5'-triphosphate were studied in rats using a quantitative Evans blue dye-leakage technique. Rats anaesthetized with either were given Evans blue. i.v. and intracutaneous injections of inflammatory agents were given into the shaved abdominal skin. Doses of substance P, 1-5 X 10(-10) mol, produced graded dye leakage. A low dose of substance P (5 X 10(-11) mol) potentiated responses to 5-hydroxytryptamine (2.5 X 10(-10) mol), bradykinin (5 X 10(-10) mol), prostaglandin E1 (5 X 10(-10) mol) and adenosine 5'-triphosphate (2.5 X 10(-7) mol) but no histamine (2 X 10(-8) mol). A higher dose of substance P (5 X 10(-10) mol) was potentiated by prostaglandin E1 (5 X 10(-11) mol) and adenosine 5'triphosphate (5 X 10(-9) mol) but but not by histamine (5 X 10(-10) mol) or bradykinin (5 X 10(-11 mol) and was inhibited by 5-hydroxytryptamine (5 X 10(-12) mol). If substance P is released from sensory nerves in some inflammatory states these interactions might be of importance in determining the response observed.
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PMID:Interactions of substance P with putative mediators of inflammation and ATP. 88 57

1. The release of PGs from the isolated perfused rabbit ear was measured by means of a radioimmunoassay. 2. Bradykinin in dose dependent amounts released mainly PGE (presumably PGE1) and in much smaller amounts also PGF. 3. Bradykinin released similar amounts of PGE in innervated and chronically denervated ears. 4. Indomethacin completely prevented the PGE release by bradykinin. 5. ACh showed a much lower efficacy than bradykinin in releasing PGE and PGF. Synthetic substance P was devoid of any PGE releasing action. 6. It is concluded that bradykinin increases its own algesic action by a concomitant rapid stimulation of the PGE synthesis, thus providing a mechanism for the facilitation of its own algesic action.
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PMID:Release of prostaglandins by bradykinin as an intrinsic mechanism of its algesic effect. 100 30

Synthetic substance P stimulated adenylate cyclase activity in particulate preparations from rat and human brain. The concentration of substance P for half maximal stimulation in rat brain was 1.8-10-minus 7 M. The stimulatory effect of substance P on the rat brain adenylate cyclase activity was 88% compared with 48% by noradrenalin, 163% by prostaglandin E1 and 184% by prostaglandin E2. Both the basal and substance P-stimulated adenylate cyclase activity in rat brain were inhibited by concentration of Ca-2+ above 10-minus 6 M. The chelating agent ethyleneglycol-bis-(beta-aminoethylether)-N, N'-tetraacetic acid at a concentration of 0.1 mM reduced the basal adenylate cyclase activity by 64% and eliminated the substance P-stimulated activity. The inhibition by ethyleneglycol-bis-(beta-aminoethylether)-N, N'-tetraacetic acid was completely reversed by increasing concentrations of Ca-2+.
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PMID:Stimulation of brain adenylate cyclase activity by the undecapeptide substance P and its modulation by the calcium ion. 112 64

1. The effects of calcitonin gene-related peptide (CGRP) and other vasoactive mediators of inflammation on blood flow in the synovial vessels and plasma protein extravasation into the knee (femoro-tibial) joint of the pentobarbitone-anaesthetized rat were measured. 2. Changes in synovial blood flow were estimated by 133xenon clearance from the synovial cavity. CGRP (0.1 pmol and 10 pmol) and prostaglandin E1 (PGE1; 3 pmol and 300 pmol) significantly increased clearance from the knee joint measured 5 min after intra-articular injection. Substance P (10 pmol) had no effect on synovial blood flow. 3. Intra-articular perfusion of the rat knee with CGRP at concentrations up to 0.1 mM, or PGE1 at concentrations up to 10 microM, did not increase plasma extravasation into the synovial cavity measured by accumulation of intravenously injected 125I-albumin in the perfusate. 4. Plasma extravasation into the knee was significantly increased by infusion of bradykinin (0.1 microM), 5-hydroxytryptamine (1 microM) and histamine (0.1 mM), compared with the contralateral joints in the same animals which were perfused with Tyrode solution. 5. Perfusion of the knee joint with substance P did not specifically induce 125I-labelled albumin accumulation in the synovial cavity even at doses that had systemic effects as observed by marked plasma extravasation into other tissues. 6. The increase in plasma extravasation induced by histamine (0.1 mM) was potentiated by co-infusion with CGRP (0.1 microM) and PGE1 (3 microM). However the response to a submaximal dose (0.1 microM) of bradykinin, which induced similar plasma extravasation to histamine (0.1 mM), was not increased by co-infusion with CGRP or PGE1.7. These results show that CGRP is a potent vasodilator in the rat knee. CGRP released from sensory nerves may act synergistically with mediators of increased vascular permeability to modify the inflammatory response in this site.
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PMID:Calcitonin gene-related peptide increases blood flow and potentiates plasma protein extravasation in the rat knee joint. 138 Mar 89

To determine whether neurogenic inflammation can be inhibited by prostaglandin E1 (PGE1), that is suggested to have an inhibitory effect on neuropeptide release from airway sensory nerves, we examined plasma extravasation in the airways of anesthetized rats in vivo with Evans blue due as a marker. Neurogenic inflammation was produced by an i.v. injection of capsaicin (100 micrograms/kg) or by antidromic electrical stimulation of the right vagus nerve (4 Hz, 1 ms, 4 V for 1 min). Capsaicin injection significantly increased leakage of dye in the trachea and main bronchi. Similar increases in leakage were seen in the trachea and right bronchus on electrical stimulation of the right vagus nerve. PGE1 (1-1000 micrograms/kg) inhibited the leakage induced by capsaicin in the trachea and bronchi concentration dependently with complete inhibition at a concentration of 1000 micrograms/kg. Likewise, PGE1 (1000 micrograms/kg) significantly inhibited electrical stimulation-induced leakage in the trachea and right bronchus (P less than 0.01). I.v. substance P (SP; 1 microgram/kg) increased Evans blue dye extravasation in the same way as the leakage induced by capsaicin and electrical stimulation but PGE1 (1000 micrograms/kg) failed to inhibit SP-induced leakage in the trachea and main bronchi (P greater than 0.20). These results suggest that PGE1 inhibits neurogenic plasma leakage by presynaptic inhibition of the release of neuropeptides from sensory nerves.
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PMID:Inhibitory actions of prostaglandin E1 on neurogenic plasma extravasation in rat airways. 138 5

Airway submucosal glands are by volume the most important source of macromolecules in airway secretions. These secretions, containing gel-forming mucins, antibacterial proteins, and antiproteases, comprise the major defensive barrier protecting the host against airborne pathogens. The identification of the mechanisms regulating secretion from the submucosal glands is key to understanding the genesis of this barrier and how it is altered by disease processes. Using a variety of methods, we and others have identified on the gland cells of several species receptors specific for ACh, norepinephrine, substance P, VIP, PGE1, PGE2, PGA1, PGD2, histamine and bradykinin. These receptors all participate in modulating the secretory activity of the airway submucosal glands. Studies of homogeneous cultures of bovine airway serous cells have yielded detailed information regarding the beta-adrenergic receptor on these cells. Using radioligand binding techniques, we found evidence for the presence of a single high affinity beta receptor of beta-2 subtype. Occupancy of this receptor by isoproterenol causes an elevation in the concentration of intracellular cAMP, which in turn stimulates the phosphorylation of a subset of cytoplasmic and membrane proteins. Based on the kinetics and pharmacology of these effects, it is likely that cAMP functions as a second messenger in the serous cell secretory pathway, probably acting through protein kinases. Current efforts are directed at identification of those phosphoproteins whose phosphorylation and dephosphorylation times are consistent with their possible roles in secretion.
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PMID:Receptors on airway gland cells. 215 62

We have investigated the effect of prostaglandin E1 (PGE1) on non-adrenergic, non-cholinergic (NANC) contraction in guinea-pig bronchial strips. PGE1 (10 nM to 10 microM) did not alter baseline tension but reduced NANC contractions induced by electrical field stimulation (EFS) in a concentration-dependent fashion (-log EC50 was 6.60 +/- 0.10 M and maximum inhibition was 88.7 +/- 2.9%). PGE1 (greater than 0.3 microM) also reduced the contraction induced by substance P (1 microM). Removal of epithelium did not alter the effects of PGE1 on NANC contraction. These results suggest that PGE1 exerts both pre- and post-junctional inhibitory actions on NANC contraction.
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PMID:Inhibitory actions of prostaglandin E1 on non-adrenergic non-cholinergic contraction in guinea-pig bronchi. 228 55

Contractile responses due to substance P released from the trigeminal nerve were observed after electrical transmural stimulation or exogenous application of bradykinin in the isolated rabbit iris sphincter muscle. Prostaglandins, particulary prostaglandin E1, enhanced and indomethacin inhibited these substance P-ergic responses. Since the responses to exogenously applied substance P were neither affected by prostaglandins nor indomethacin, it was suggested that prostaglandins acted presynaptically to enhance the release of substance P from the trigeminal nerve terminals.
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PMID:Prostaglandins enhance trigeminal substance P-ergic responses in the rabbit iris sphincter muscles. 241 36


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