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)

To determine the mechanism by which substance P (SP) activates human neutrophils, we examined the potencies of SP, the C-terminal peptides SP4-11 and SP6-11, and the N-terminal peptides SP1-9 and SP1-4 for inducing the increase in cytosolic free Ca2+ concentration ([Ca2+]i), superoxide (O2-) generation, and chemotaxis in human blood neutrophils. SP and the C-terminal peptides SP4-11 and SP6-11 and SP6-11 (10(-6)-10(-4) M) induced the increase in ([Ca2+]i, O2- generation, and chemotaxis of the neutrophils dose--dependently, whereas the N-terminal peptides SP1-9 and SP1-4 (up to 10(-4) M) were inactive in inducing these responses. Furthermore, the potencies of the two C-terminal peptides SP4-11 and SP6-11 were not parallel in these three responses. SP6-11 was 7.7-fold more potent in increasing [Ca2+]i than SP4-11, whereas SP4-11 was 16.6-fold more potent in inducing O2-generation than SP6-11. SP6-11 was also 2.1-fold more potent in inducing chemotaxis than SP4-11. Thus, we conclude that the C-terminal peptides of SP induce differential activations of human neutrophils.
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PMID:Differential effects of two C-terminal peptides of substance P on human neutrophils. 170 Dec 27

The effects of unilateral injections of two substance P fragments, the N-terminal substance P (1-7) (SP1-7) and the C-terminal substance P (6-11) (SP6-11) into the substantia nigra, pars reticulata on dopamine (DA) release in the ipsilateral striatum of halothane-anaesthetized rats were studied using microdialysis. SP1-7 and SP6-11 were also tested for their ability to modify the DA stimulation produced by intranigral injections of SP or neurokinin A (NKA). In addition, the SP antagonist Spantide I was tested for its ability to modify the DA stimulation produced by an intranigral injection of SP1-7. Intranigral injections of SP1-7 (0.001-5.0 nmol) inhibited DA release after low doses (0.001-0.01 nmol), but stimulated DA release after high doses (0.1-5.0 nmol). Striatal dihydroxyphenylacetic acid (DOPAC) levels increased moderately after high doses of SP1-7 (1.0-5.0 nmol). Intranigral injections of SP6-11 (0.01-5.0 nmol) inhibited DA release, but enhanced striatal DOPAC levels, dose-dependently. SP1-7 (0.01-0.1 nmol), but not SP6-11 (0.1 nmol), blocked the stimulation of striatal DA release produced by intranigral SP (0.07 nmol). Neither SP1-7 (0.1 nmol) nor SP6-11 (0.1 nmol) could modify the stimulation of striatal DA release produced by intranigral NKA (0.09 nmol). The increase in DA release after a high dose of SP1-7 (1.0 nmol) was not modified by co-administration with Spantide I (0.07 nmol).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intranigral substance P modulation of striatal dopamine: interaction with N-terminal and C-terminal substance P fragments. 170 82

The N-terminal tetrapeptide of substance P (SP1-4) was found to produce analgesia, after the icv injection to the rat brain, which is lower in its intensity than that produced by tuftsin (Thr-Lys-Pro-Arg tetrapeptide). Among investigated tuftsin analogues Thr-Lys-Pro-Thr and Thr-Lys-Pro-Thr-Asp (partial sequences of S-protein of HB virus) were weakly active, Thr-Arg-Pro-Arg was inactive, and Thr-Lys-Pro-Gly-Arg produced a weak hyperalgesia 30 min after the icv injection. The obtained results were compared with those obtained previously in the phagocytosis stimulation test. In the control experiments the effects of free amino acids of the tuftsin molecule (Thr, Lys, Pro, Arg) were also studied.
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PMID:Antinociceptive action of the SP1-4 tetrapeptide and of some tuftsin analogs. 171 Nov 98

The tachykinins substance P (SP) and neurokinin A are believed to be major mediators of neurogenic inflammation. To determine whether the skin reactivity to tachykinins is increased in asthmatics, we examined the erythemas and wheals induced by intradermal injections of SP, the C-terminal peptide SP6-11, the N-terminal peptide SP1-9 and neurokinin A (10(-7)-10(-5) M) in 10 allergic asthmatics and 9 normal subjects. SP and SP1-9 induced both erythemas and wheals in a concentration-dependent manner in allergic asthmatics and in normal subjects, whereas SP6-11 and neurokinin A induced only wheals in both groups. SP induced greater erythemas and wheals in allergic asthmatics than in normal subjects. However, the wheals induced by neurokinin A were not significantly different between the two groups. SP1-9 also induced greater erythemas and wheals in allergic asthmatics than in normal subjects, whereas the wheals induced by SP6-11 were not significantly different between the two groups. Therefore, the increased skin reactivity to SP was dependent on the N-terminal peptide but not on the C-terminal peptide. We conclude that the skin reactivity to SP but not to neurokinin A is increased in allergic asthmatics.
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PMID:Skin reactivity to substance P, not to neurokinin A, is increased in allergic asthmatics. 171

1. We have used synaptosomal membranes to study the influence of substance P and its fragments and analogues of its C-terminal fragment on Ca2+/calmodulin-dependent synapsin I endogenous phosphorylation. 2. SP1-11, SP1-4, [Tyr8]SP6-11 and [pGlu6, Tyr8]SP6-11 at 10(-3) M greatly inhibited synapsin I phosphorylation. 3. SP6-11 at all investigated concentrations and SP1-11, SP1-4, [Tyr8]SP6-11, [pGlu6, Tyr8]SP6-11 at 10(-4) and 10(-5) M were ineffective. 4. The results indicate that SP1-11 and its N-terminal fragment and analogues of its C-terminal fragment act on the phosphorylation of specific synaptic protein (synapsin I) and therefore may influence the release of neurotransmitters, membrane conductance and potentiation or inhibition of other signalling systems.
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PMID:Substance P and its fragments affect Ca2+/calmodulin-dependent synaptosomal membrane protein phosphorylation from rat cerebral cortex. 172 84

The purpose of this investigation was to examine the pathway of substance P (SP) and neurotensin (NT) catabolism in the gastric wall of the rat and identify some of the enzymes involved. Under anaesthesia an infusion catheter and a bundle of dialysis fibres were implanted into the stomach wall of the rat. Experiments commenced on conscious rats 2 days after surgery. In control experiments [3H]-SP(Pro-2,4) or [3H]-NT(Tyr-3,11) were injected into gastric tissues through the catheter and catabolites were collected in the dialysis fibres and separated by high pressure liquid chromatography. In other studies captopril, MK422 (inhibitors of angiotensin converting enzyme) or phosphoramidon (an inhibitor of endopeptidase-24.11, 'enkephalinase') were injected into gastric tissues before the peptide label. SP1-11 was degraded to mainly SP1-2, SP3-4 with some SP1-6, SP1-7 and SP1-8. Catabolism was partially but significantly (5% level) inhibited by MK422 and captopril, but not by phosphoramidon. NT1-13 was degraded to NT1-8, NT9-13, NT1-11 and NT1-12. NT catabolism was partially but significantly (5% level) inhibited by MK422. It is concluded that an enzyme resembling angiotensin converting enzyme is involved in the initial stages of SP and NT catabolism in the rat stomach. The involvement of other peptidases cannot be excluded because inhibition of breakdown was not complete.
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PMID:Catabolism of substance P and neurotensin in the rat stomach wall is susceptible to inhibitors of angiotensin converting enzyme. 242 51

Substance P and the N-terminal sequences SP1-9, SP1-7, SP1-4 and SP1-2 were investigated in their action on stress related alterations in blood pressure behaviour, stress related disturbances in conditioned reflex learning behaviour, alterations in the endogenous opioid system and on the blood pressure behaviour of spontaneously hypertensive rats. In addition the occurrence of vegetative effects such as acute hypertension and histamine release from mast cells were investigated. The results of this work show that N- and C-terminal sequences of the Substance P molecule differ in their actions. Whereas the vegetative effects decrease if the SP molecule is shortened from the C to the N-terminus the "antistress effect" of the Substance P molecule remains unchanged. Whereas the N-terminal tetrapeptide SP1-4 can be considered "essential" for the "antistress effect", the C-terminal pentapeptide of SP is considered to be the "essential sequence" for the vegetative effects. These results will open new possibilities for the synthesis of selectively acting SP-agonists.
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PMID:[The role of the N-terminal of the substance P molecule in its action in stress-related behavioral and blood pressure disorders]. 243 39

Selye found that in response to different stressors the body reacts with a characteristic stress syndrome: adrenal enlargement, gastrointestinal ulcera, and thymicolymphatic involution. In this paper we demonstrate that i.p. injected Substance P (SP) can prevent stress-induced involution of thymus in Wistar rats. This protecting effect on the immune system of SP, in addition to the "normalizing" effects of this peptide on stress-induced disorders in vegetative and central functions first described by Oehme and co-workers and Hecht and co-workers is a new hint to the function of SP as an "anti-stress" agent. The mode of action of the anti-stress effect of SP in adrenals as well as in the thymus is discussed. It is suggested that the anti-stress effect of SP1-11 and its N-terminal fragment SP1-4 is mediated by specific receptors in adrenals and/or thymus which are different from the so called SP-P and SP-E receptors.
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PMID:Prevention of stress-induced involution of the thymus in rats by substance P (SP1-11) and its N-terminal fragment SP1-4. 243 98

In the present paper the effects of substance P (SP1-11, Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-MetNH2) and delta sleep inducing peptide (DSIP, Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) to normalize the deprivation of sleep in chronically stressed rats with hyposomnia were investigated. The results indicated that SP1-11 is more potent than DSIP in rats with stress-induced hyposomnia. Different effects were found in the duration of sleep, the percentage of sleep phases compared to wake phases, the rhythm of sleep phases and the time periods of sleep-cycles. Based on the present results both the common and differences in the mode of action were discussed.
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PMID:[Comparison of the effects of DSIP and SP 1-11 on stress-induced chronic sleep disorders in rats]. 244 61

The ability of the SP fragments SP2-11 and SP3-11 to release histamine from rat peritoneal mast cells has been compared with that of the whole peptide. SP1-11 was found to be about 3.4 times more active than SP2-11 and about 10.4 times more active than SP3-11. The substance P antagonist [D-Pro4, D-Trp7,9,10] SP4-11 was equally effective at antagonizing the histamine releasing action of SP1-11, SP2-11 and SP3-11. Benzalkonium chloride was found to be a competitive antagonist of SP and SP3-11: the dissociation constants for the benzalkonium chloride-receptor interaction being about the same when either SP1-11 or SP3-11 was used as the agonist.
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PMID:Action of the SP2-11 and SP3-11 fragments of substance P on rat peritoneal mast cells. 244 Feb 65


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