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)

We report the development of a sensitive and specific radioimmunoassay for substance P based on a new extraction technique for this peptide. In this technique, substance P-like immunoreactivity (SPLI) was extracted from midly acidified plasma successively with 0.05M ammonium sulfate and ethanol; recovery was almost quantitative (89.5 +/- 3.2%) and was independent of concentration. Basal substance P levels averaged 22 +/- 3 pg/ml in 33 dogs. Following initiation of a high-protein meal, mean SPLI levels in three dogs (in a total of 12 experiments) increased significantly from 26 +/- 3 to a peak of 37 +/- 4 pg/ml at 15 minutes, after which they slowly returned to the initial levels.
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PMID:Radioimmunoassay measurement of substance P release following a meat meal. 616 4

Acute administration of ethanol can potentiate the inhibitory effects of exogenously administered opioids on release of acetylcholine from the guinea pig's enteric nervous system. Ethanol also appears to inhibit the release of enteric substance P by enhancing the inhibitory action of simultaneously released endogenous opioids. One consequence of this mechanism of action is that those states that result in the activation of opioid-containing systems, such as stress, might also be the conditions under which the opioid component of the actions of ethanol are the most pronounced.
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PMID:Opioid-mediated acute responses to alcohol: ethanol potentiates opioid actions on the guinea pig ileum. 619 73

These studies were designed to determine the effects of castration and ethanol (ETOH) on the relative content of substance P (SP) immunoreactivity in the hypothalamus and the central and medial amygdaloid nuclei (CM-AM). Differences visualized immunocytochemically between saline-treated intact and castrated rats indicated that a visible decrease in the number and intensity of immunostained fibers within the CM-AM occurred following castration. Conversely, the number of labeled fibers and the intensity of the reaction product was greater in castrated rats treated with ETOH as compared to the castrated rats receiving only saline. In ETOH-treated intact animals, the number of SP-containing fibers of the CM-AM was slightly greater than the saline-treated intact controls. Similar results were seen for specific regions of the hypothalamus although they were less pronounced than that visualized in the CM-AM. These data indicate that both castration and administration of ETOH affects hypothalamic and amygdaloid content of SP, and also suggests that ETOH may diminish the release of SP. Possible interactions between SP and luteinizing hormone-releasing hormone are discussed.
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PMID:Effects of castration and ethanol on amygdaloid substance P immunoreactivity. 620 91

By acid extraction, ethanol precipitation, affinity chromatography on 4-phenylbutylamine-Sepharose 4B and gel filtration on Sephadex G-100, calf liver neutral proteinase was purified. The purified enzyme was electrophoretically homogeneous and over 2000 times more active than the starting homogenate. The molecular weight, determined by SDS electrophoresis, was calculated as 27000. The pH optimum of the enzyme for whole calf thymus histones and N-benzoyltyrosine, ethyl ester (BTEE) was at 7.0 and 7.0-7.5. The Km value for histones was 2% and for BTEE 1.66 mM. The enzyme was strongly inhibited by soya-bean trypsin inhibitor and leucocyte intracellular I-1A inhibitor and less by alpha 1-antitrypsin and leucocyte inhibitor I-1B. The enzyme hydrolyzed only selected protein substrates, such as total thymus histones, Lys-rich histones, nucleoprotein and substance P, but not Arg-rich histones, hemoglobin and casein. The enzyme showed chymotrypsin-like properties by cleavage of substance P at the carboxyl groups of phenylalanine and leucine.
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PMID:The isolation of liver serine proteinase by affinity chromatography on 4-phenylbutylamine-sepharose 4 B. 705 3

N1E-115 mouse neuroblastoma cells were used to study the influence of ethanol on the 5-HT- and veratridine-induced influx of 14C-guanidinium via the 5-HT3 receptor channel and the fast sodium channel, respectively. Ethanol (10-100 mM) concentration-dependently increased the 5-HT-induced 14C-guanidinium influx, leaving the basal and veratridine (100 microM)-induced influx unaffected. The increasing effect of ethanol (100 mM) was observed at all 5-HT concentrations investigated; accordingly, ethanol increased the maximum response to 5-HT. Whereas in the absence of ethanol the concentration-response curve for 5-HT was bell-shaped, this was no longer the case when ethanol (100 mM) was present in the incubation buffer; the descending branch of the concentration-response curve for 5-HT at concentrations above 300 microM was virtually no longer observed. When, in the presence of substance P (10 microM) the 5-HT-induced 14C-guanidinium influx was already enhanced, the ability of ethanol (100 mM) to increase the 5-HT-induced influx was considerably diminished (by 72%). Preincubation of N1E-115 cells with 5-HT caused a decay of the subsequent 5-HT response ("desensitization") which was dependent on the duration of preincubation; ethanol (100 mM) did not affect the rate of this decay of the 5-HT response. The 5-HT (30 microM)-induced 14C-guanidinium influx was also increased by methanol (100 mM) and n-propanol (100 mM). The rank order of the increasing effect of the n-alkanols (at 100 mM) was: methanol < ethanol < n-propanol; i.e. the degree of enhancement increased with the lipophilicity of the alcohols.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increasing effect of ethanol on 5-HT3 receptor-mediated 14C-guanidinium influx in N1E-115 neuroblastoma cells. 747 37

The dynorphin A (1-17), Met-enkephalin-Arg6-Phe7 and substance P levels were determined by RIA following Sep-Pak separation in the striatum, hippocampus and spinal cord of three strains of mice (C57Bl10/D1, A/Sn, A. CA). The C57Bl10/D1 mice had high consumption of 10% ethanol at free choice schedule, whereas the A/Sn and A. CA mice had very low one. The Met-enkephalin-Arg6-Phe7 level was found to be decreased only in the spinal cord and striatum of C57Bl10/D1 mice. It is suggested that decreased synthesis or processing of the proenkephalin may at least partly determine the high level of ethanol consumption by this strain of mice.
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PMID:[The content of dynorphin, Met-enk-Arg6-Phe7 and substance P (1-11) in the brain of mice with different levels of ethanol consumption]. 750 73

The present study evaluated the effect of tachykinin agonists, selective for different neurokinin (NK) receptors, on alcohol intake in genetically selected, Sardinian alcohol-preferring rats. Tachykinins were given by intracerebroventricular injection just before access to fluids. In rats offered both water and 8% ethanol 2 h/day, the NK3 selective agonists [Asp5.6,MePhe8]substance P(5-11), Suc[Asp6,MePhe8]substance P(6-11), and [MePhe7]neurokinin B markedly suppressed alcohol intake. The NK1 selective agonist [Sar9,Met(O2)11]substance P and the NK2 selective agonist GR 64349 did not At doses that inhibited alcohol intake, the NK3 agonists did not modify water intake; total fluid intake was significantly reduced only following 500 ng/rat of [Asp5.6,MePhe8]substance P(5-11). When rats were given a longer access to fluids (8% alcohol for 2 h, but water for 4 h), again, NK3 agonists suppressed alcohol intake, but not total fluid intake. Moreover, NK3 agonists did not modify solid food intake in food-deprived rats, nor water intake in water-deprived rats, when alcohol was not available. These findings indicate that NK3 agonists inhibit alcohol intake in Sardinian alcohol-preferring rats and that their effect is behaviorally selective. They also suggest that central NK3 receptors may be involved in alcohol intake control in rats.
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PMID:Selective agonists at NK3 tachykinin receptors inhibit alcohol intake in Sardinian alcohol-preferring rats. 750 13

The interrelationship between somatostatin and its synthetic analog, sandostatin, with neuropeptides and inflammatory mediators, as well as their protection of gastric mucosal damage, were tested in rats. Rats were treated intragastrically with 1.0 ml of 96% ethanol with or without intravenous or intraperitoneal coadministration of somatostatin (1.0 microM/kg). Mucosal damage was also induced by the administration of either indomethacin (30 mg/kg subcutaneously) with or without intravenous sandostatin (10 micrograms/rat), given 30 min prior to damage induction. Somatostatin levels in ethanol-damaged gastric mucosa were significantly lower than in control rats. Substance P and vasoactive intestinal peptide (VIP) levels were significantly higher in the damaged mucosa in rats treated with ethanol, as was the mucosal generation of leukotriene B4 (LTB4) and cysteinyl-containing leukotrienes. The coadministration of somatostatin with ethanol significantly reduced gastric mucosal injury induced by ethanol alone. The protection of the mucosa was accompanied by reduction of mucosal substance P and VIP levels, as well as the generation of leukotrienes, an effect that was reversed by intraperitoneal or intravenous coadministration of somatostatin antagonist, cyclo-(7-aminoheptanoyl-PH-E-D-Trp-Lys-THR), 1.0 microM/100 g, with somatostatin (1.0 microM/kg) and ethanol. When given by itself somatostatin significantly reduced mucosal leukotriene generation compared with their generation in saline-treated rats. Sandostatin completely abolished gastric mucosal damage induced by indomethacin administration. In rats treated with somatostatin and indomethacin, this effect was accompanied by reduction of mucosal leukotriene generation. Administration of sandostatin to pylorus-ligated rats significantly reduced gastric acid output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatostatin effectively prevents ethanol- and NSAID-induced gastric mucosal damage in rats. 751 Jun 7

The present study determined the participation of different endogenous mediators in adaptive cytoprotection against gastric gland damage caused by ethanol in rabbits. Using the isolated gland preparation, pretreatment with 10(-5)M of either indomethacin, Nw-nitro-L-arginine methyl ester (L-NAME) or N-ethylmaleimide (NEM), but not of substance P antagonist, intensified the 10% (v/v) ethanol-induced gastric gland damage and lessened the degree of cytoprotection evoked by 2% (v/v) ethanol to a significant level. Co-administration with 10(-4)M of prostaglandin E2, L-arginine or glutathione to the respective groups completely reversed the above adverse effects. These results demonstrate the involvement of endogenous prostaglandins, nitric oxide and glutathione in gastric adaptive cytoprotection against the damaging action of ethanol in the rabbit gastric glands.
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PMID:Endogenous mediators in adaptive cytoprotection against ethanol-induced gastric gland damage in rabbits. 753 Mar 12

To explore the mechanisms of airway hyperreactivity to aerosolized substance P observed in guinea pigs 14 days after intratracheal injection of sulfur mustard (SM), we studied the effects of epithelium removal and inhibition of neutral endopeptidase (NEP) activity on airway muscle responsiveness. Tracheal rings from SM-intoxicated guinea pigs expressed a greater contractile response to substance P than rings from nonintoxicated guinea pigs. After epithelium removal or incubation with the NEP inhibitor phosphoramidon, the contractile responses of tracheal rings to substance P did not differ in guinea pigs injected with SM or ethanol (SM solvent). Treatment of the guinea pigs with betamethasone for 7 days before measurement abolished the airway muscle hyperresponsiveness observed in untreated SM-intoxicated guinea pigs and partially restored tracheal epithelium NEP activity. In addition, the tracheal epithelium height and cell density of SM-intoxicated guinea pigs treated with betamethasone were significantly greater than in those without betamethasone. These results demonstrate that SM intoxication induces airway muscle hyperresponsiveness to substance P by reducing tracheal epithelial NEP activity and that glucocorticoids might inhibit this hyperresponsiveness by increasing this activity.
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PMID:Glucocorticoids inhibit sulfur mustard-induced airway muscle hyperresponsiveness to substance P. 753 48


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