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)

The effects of the putative neurotransmitters acetylcholine, adrenaline, adenosine, ATP, bombesin, 5-hydroxytryptamine, met-enkephalin, neurotensin, somatostatin, substance P and VIP have been investigated in the perfused intestine of the cod, Gadus morhua. The presence and distribution of the different types of nerves was investigated with immunohistochemistry and Falck-Hillarp fluorescence histochemistry. A spontaneous rhythmic activity of the perfused preparations usually occurred within a few minutes from the start of the experiment. This activity was diminished or abolished by addition of atropine, methysergide or tetrodotoxin to the perfusion fluid. Acetylcholine, 5-hydroxytryptamine or substance P caused a contraction of the intestinal wall. The response to acetylcholine was blocked by atropine but not by tetrodotoxin, while the response to 5-hydroxytryptamine was blocked by methysergide and usually also by tetrodotoxin. This indicates that the effect of acetylcholine is direct on the muscle cells, while the effect of 5-hydroxytryptamine may be at least partly via a second neuron. All adrenergic agonists (adrenaline, isoprenaline and phenylephrine) had a dominating inhibitory effect on the intestine. Experiments with antagonists showed that the inhibition is due to stimulation of both alpha-adrenoceptors and beta-adrenoceptors. ATP, adenosine and somatostatin also caused a relaxation of the intestinal wall, often followed by a contraction. Met-enkephalin produced variable responses, either a relaxation, a contraction or both. Bombesin caused a weak inhibition, if anything. Neurotensin and VIP did not visibly affect the intestinal motility. 5-HT-, substance P- and VIP-like immunoreactivity and catecholamine fluorescence were observed in the myenteric plexus, submucosa and muscle layers in all parts of the intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurotransmitters in the intestine of the Atlantic cod, Gadus morhua. 241 59

In helical strips cut from the small mesenteric artery of guinea-pig (GPSMA) (0.3-0.6 mm o.d.) relaxations induced by substance P were more susceptible to damage of the endothelium by rubbing than were relaxations evoked by carbachol. Relaxations induced by 2-nicotin-amidoethyl nitrate (SG75) were unaffected by this procedure. Relaxations evoked by the calcium ionophore A23187 persisted when those to substance P had been abolished by rubbing the endothelium in GPSMA, rabbit mesenteric and rabbit ear arteries. In guinea-pig pulmonary artery and aorta relaxations to A23187 were lost after this treatment. Carbachol and SG75 were more effective in inhibiting phasic than tonic tension induced by noradrenaline in GPSMA, but substance P was more effective against tonic tension. In the GPSMA, carbachol and substance P inhibited tension produced by noradrenaline to similar extents. However, carbachol was less, and substance P much less effective in inhibiting tension evoked by high-potassium solution than by noradrenaline. Susceptibility of relaxations to blockade by haemoglobin in GPSMA was: substance P greater than carbachol greater than ATP greater than SG75. The membrane potential of smooth muscle cells in the media of the GPSMA was recorded by microelectrode. Carbachol, but not substance P, hyperpolarized the cells both in the presence and absence of noradrenaline at concentrations which relaxed the muscle. These results suggest a heterogeneity in the mechanisms of endothelial-dependent relaxations induced by various vascular relaxants.
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PMID:Endothelial-dependent relaxant actions of carbachol and substance P in arterial smooth muscle. 242 70

The apomorphine-induced inhibition of histamine release in rat peritoneal mast cells was studied by means of secretagogues stimulating different pathways of mast cell activation. Apomorphine inhibited the mast cell response to all releasing agents (lysophosphatidylserine plus nerve growth factor, compound 48/80, substance P, ATP, tetradecanoylphorbolacetate, melittin). The IC50 ranged from 4 microM to 24 microM at concentrations of secretagogues releasing 30-50% of mast cell histamine. However, the potency of the drug decreased at higher secretagogue concentrations. Mast cells, pretreated with apomorphine and washed, released little histamine upon stimulation. The secretory response could be partially restored on increasing the concentration of secretagogues. The results suggest that apomorphine affects a regulatory step controlling the terminal sequence of mast cell secretory activity. As indicated by the reduced potency of the drug, the control by the apomorphine-sensitive reaction loses efficiency under conditions of massive histamine release.
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PMID:Apomorphine-induced inhibition of histamine release in rat peritoneal mast cells. 242 81

A bland procedure, conducted in ice, is described for the extraction with HCl of smooth-muscle-contracting substances from plexus-containing ileal longitudinal muscle (l.m.) sheets obtained mainly from rabbits and some guinea-pigs. The spasmogenic activity in rabbit extracts was distinguished from acetylcholine, histamine and 5-hydroxytryptamine by antagonists; and from prostaglandins, by its insolubility in ether at acid pH and by pretreatment of the animals with indomethacin. The fact that it contracts the separated l.m. of the guinea-pig ileum, whether plexus-containing or plexus-free, and in atropine distinguishes it also from methionine-enkephalin, somatostatin, 13-norleucine motilin, bombesin, and cholecystokinin octapeptide (CCK8). This activity was partially purified, first by several partitions with ether at pH 1.4-2.2 and then by treatment at pH 4.5-5 with lead acetate. The virtual absence of ATP was confirmed by the firefly bioluminescence technique. The guinea-pig-ileum-contracting component in the partially purified extracts was destroyed by pepsin, chymotrypsin and DPCC-treated trypsin, indicating its peptide nature and distinguishing it from oxytocin, vasopressin, bradykinin, etc. In parallel assays the partially purified rabbit extracts were considerably more active than Substance P on jird or rat ascending colons than on the guinea-pig l.m., suggesting the presence of a second spasmogenic component in the extracts. In guinea-pig extracts the partially purified activity was 8-16 times greater when plexus-containing than when plexus-free, pointing to Auerbach's plexus as the source of the activity.
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PMID:Extraction and partial purification of spasmogenic substances in Auerbach's plexus. 242 21

The cholinergic and noncholinergic-nonadrenergic (NCNA) excitatory and inhibitory responses of the guinea-pig ileum to transmural nerve stimulation (TNS) were studied. Unlike the contraction induced by histamine and acetylcholine the responses to TNS, ATP, substance P, bradykinin, 5-HT and GABA were not sustained. The contraction and its fading during TNS involved the activation of cholinergic, adrenergic and NCNA neurons. Substance P, 5-HT and ATP desensitization resulted in reduction of the excitatory NCNA response whereas that due to bradykinin attenuated both the excitatory and inhibitory NCNA responses. The desensitization against TNS and the potential transmitters studies was selective except in the case of ATP. The present results suggest that it is unlikely that ATP, bradykinin or GABA would be the NCNA transmitters in the guinea-pig ileum. The cross-desensitization between the excitatory NCNA transmitter on the one hand, and substance P (markedly expressed) and 5-HT (slightly expressed) on the other hand, give further evidence in favor of the possible transmitter role of substance P-like peptide in excitatory NCNA transmission and of the role of 5-HT in the activation of NCNA neurons.
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PMID:Effect of desensitization induced by adenosine 5'-triphosphate, substance P, bradykinin, serotonin, gamma-aminobutyric acid and endogenous noncholinergic-nonadrenergic transmitter in the guinea-pig ileum. 242 32

The contribution of the myenteric plexus in the mechanical responses of rat jejunal longitudinal muscle produced by several enteric nerve substances was evaluated. The myenteric plexus of a segment of rat jejunum was destroyed by serosal application of benzalkonium chloride (BAC). Fifteen days after BAC treatment, both the BAC-treated and an orad control jejunal segment were removed and the mechanical responses of the longitudinal muscle produced by the following substances were examined: substance P, acetylcholine (ACh), 5-hydroxytryptamine (5-HT), cholecystokinin octapeptide (CCK-8), norepinephrine, vasoactive intestinal peptide (VIP), bombesin, [Leu5]enkephalin and somatostatin. Our results indicate that: substance P and norepinephrine produce their mechanical responses by acting predominantly on the longitudinal smooth muscle; 5-HT, CCK-8, ATP, VIP and neurotensin act predominantly through the myenteric plexus; ACh possesses both direct and indirect actions; and because the responses to [Leu5]enkephalin, bombesin and somatostatin were equivocal, a conclusion as to their site of action could not be made with this preparation.
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PMID:Differentiation between myenteric plexus and longitudinal muscle of the rat jejunum as the site of action of putative enteric neurotransmitters. 243 41

The effects of injecting ATP, ADP, AMP, adenosine and adenine intrathecally on the pain response induced by the injection of substance P (10 ng/mouse) intrathecally were studied. All the compounds except adenine inhibited the pain response in a dose-related manner. The ED50 values of ATP, ADP, AMP and adenosine were 2.10, 0.93, 0.88 and 0.48 micrograms/mouse, respectively. Pretreatment with theophylline at a dose of 100 mg/kg p.o. markedly diminished all the antinociceptive effects. The effect of adenosine was not affected by s.c. injection of naloxone. These results suggest the existence of adenosine receptors which modulate spinal nociceptive sensory processing, independently of the endogenous opiate system.
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PMID:Spinal antinociceptive effects of adenosine compounds in mice. 244 Jul 5

The cross influence of polypeptides (substance P, eledoisin) and neurotransmitters (acetylcholine, histamine, 5-hydroxytryptamine, ATP) on isolated guinea pig ileum involved a reduction or loss of muscle sensitivity. After the desensitization induced by one of the neurotransmitters the sensitivity of the ileum longitudinal muscle to polypeptides as estimated by the dissociation constant of the drug-receptor complex, decreased, i.e. a non-specific cross desensitization occurred. 5-hydroxytrpyptamine, however, increased the sensitivity to the polypeptides. A similar sensibilizing effect is characteristic of the polypeptides which, after application, increased 1.5-2.0-fold the height of the maximum muscle contraction and decreased 2-4-fold the dissociation constant. A possible involvement of polypeptides not only in their interaction with the target cells but also in the modulation of neurotransmitters, is discussed.
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PMID:[Reciprocal effect of polypeptides and mediators on the ileum of the guinea pig]. 244 Jul 34

Plasma protein extravasation was studied in the rat abdominal skin. Substance P (SP), neurokinin A (NKA) and B (NKB) were found to induce extravasation with a threshold dose of about 1 pmol. Calcitonin gene-related peptide (CGRP) caused no or little extravasation alone but it potentiated the action of SP, NKA, NKB, and physalaemin. The potentiation of the SP-induced extravasation was unaffected by pretreatment with capsaicin, indomethacin or compound 48/80, it was reduced by neuropeptide Y or pretreatment with mepyramine plus cimetidine, and was abolished in streptozotocin diabetic rats. CGRP augmented extravasation induced by histamine, reduced the effect of ATP or adenosine and did not alter extravasation by serotonin, bradykinin or neurotensin. These results indicate that in addition to SP the novel mammalian tachykinins NKA and NKB may be considered as mediator candidates for neurogenic plasma extravasation. CGRP is a possible mediator of antidromic vasodilation. Furthermore, CGRP potentiates the extravasation caused by coexisting tachykinins and could thereby augment neurogenic inflammation. The diverse interactions of CGRP with other inflammatory mediators suggest multiple sites of action.
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PMID:Several mediators appear to interact in neurogenic inflammation. 244 66

1 Capsaicin (Cap) enhanced the twitch response of the epididymal and prostatic portions of rat vas deferens induced by field stimulation at 0.1 Hz. The effect of Cap was reproducible and showed no desensitization. 2 Prazosin, and pretreatment with reserpine or Cap did not affect the potentiating effect of Cap, whereas pretreatment with 6-hydroxydopamine abolished the action of Cap. 3 Cap tended to attenuate the contractions induced by noradrenaline, tyramine and ATP. 4 Like Cap, substance K and substance P augmented the twitch response without causing desensitization, but their effects differed somewhat from that of Cap. Calcitonin gene-related peptide inhibited the twitch response. 5 These results suggest that Cap enhances a stimulation-induced, prazosin-resistant non-adrenergic twitch response of rat vas deferens through an as yet undefined prejunctional mechanism. This mechanism is possibly mediated by some peptide released in response to Cap from sensory neurones, which in turn acts on sympathetic nerves and increases stimulation-induced release of a mediator or cotransmitter responsible for the non-adrenergic twitch response. However, the possibility that Cap has a direct action on sympathetic nerves cannot be ruled out.
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PMID:Capsaicin enhances the non-adrenergic twitch response of rat vas deferens. 244 7


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