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 isolated, hemisected spinal cord of the frog has been used to examine the action of peptides on frogs motoneurons. Both sucrose gap recording from the ventral roots and intracellular microelectrode recording were used. Substance P (SP), thyrotropin-releasing hormone (TRH), neurotensin and bombesin all had a depolarizing action. The responses to neurotensin and bombesin were blocked by tetrodotoxin suggesting that their action was indirectly mediated through interneurons. SP and TRH had a direct depolarizing action on motoneurons. SP was slightly more active and TRH slightly less active than glutamate. The responses to both peptides had a slower time course than the responses to glutamate. The maximum depolarizations produced by the peptides rarely surpassed the firing threshold of the motoneurons. However, their excitability was increased, since subthreshold synaptic potentials and responses to current injection surpassed threshold during the peptide responses. In approximately half of the cells tested, a small decrease in membrane resistance could be detected during the peptide responses. These results suggest that if SP and TRH were released from synapses impinging on frog motoneurons they would exert a background excitatory action.
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PMID:The action of thyrotropin-releasing hormone, substance P and related peptides on frog spinal motoneurons. 10 26

An enzyme which catalyzes the deamidation of thyroliberin (TRF; less than Glu-His-Pro-NH2) has been purified 110-fold from extracts of bovine anterior pituitary by ammonium sulfate fractionation, ion exchange chromatography on DEAE-cellulose, and gel filtration. This enzyme of 76,000 molecular weight (as estimated by gel filtration) exhibits maximal activity at neutral pH (optimum pH 7.4 to 7.6) in buffers of high ionic strength supplemented with thiol-protecting agents. As indicated by the strong inhibition of the enzymatic activity by N-ethylmaleimide and Hg2+, as well as by the extreme sensitivity toward diisopropyl fluorophosphate, -SH, and -OH residues apparently represent essential functional groups of the enzyme. The stereospecific deamidation of TRF (Km = 4.1 . 10(-4) M) is inhibited competitively by TRF analogues which contain proline or by the proline containing biologically active peptides luliberin (LH-RF), oxytocin, vasopressin, angiotensin II, and Substance P. TRF analogues without proline or peptide amides without proline are ineffective. This enzyme cleaves the appropriate Pro-X bonds in luliberin, angiotensin II, pyroGlu-His-Pro-Gly-NH2, and the collagenase substrate Z-Gly-Pro-Leu-Gly-Pro. Thus, it may be characterized as a post-proline-cleaving enzyme.
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PMID:Characterization of "thyroliberin-deamidating enzyme" as a post-proline-cleaving enzyme. Partial purification and enzyme-chemical analysis of the enzyme from anterior pituitary tissue. 11 64

Administered by either intravenous (i.v.) or intracisternal (i.cis.) injections, MK-771 and TRH induced a dose-related increase in EMG activity recorded from the flexor ulnaris muscle in pentobarbital-anesthetized rats. By the i.v. route, MK-771 was 6 times more potent than TRH and with i.cis. administration MK-771 was some 30 times more active than TRH. At equieffective doses of the two peptides, MK-771 exhibited a greater (approximately 3 fold) duration of action than TRH. In unanesthetized, spinally transected rats MK-771 was also more potent than TRH in eliciting EMG activity recorded from the biceps femoris muscle. Substance P, administered by the i.cis route failed to induce EMG activity. Intracisternally administered neurotensin, which did not affect EMG activity by itself, antagonized the actions of MK-771 while somatostatin was inactive in this regard. Neurotensin did not affect the EMG activity induced by physostigmine. While these studies do not delineate the mechanism whereby TRH and MK-771 induce EMG activity, it appears reasonable to suggest that TRH and related peptides, such as MK-771, may have some influence in functional disorders of human muscle.
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PMID:MK-771-induced electromyographic (EMG) activity in the rat: comparison with thyrotropin releasing hormone (TRH) and antagonism by neurotensin. 11 37

Chemical properties of substance P in the spinal cord and dorsal roots of the cat were examined by gel chromatography and paper electrophoresis. The results suggest that the substance is identical with the undecapeptide, hypothalamic substance P, recently isolated from bovine hypothalamus. Distribution of substance P in the cat spinal cord (L5-S1) was investigated. Substance P was highly concentrated in the dorsal horn, where the highest level was found in the dorsal part. After the unilateral ligation and/or section of the dorsal roots, the level of substance P in the dorsal horn, particularly in its dorsal part, was markedly lowered. In the ligated and sectioned dorsal root, substance P was highly accumulated on the ganglion side, whereas its level was lowered on the central side of the ligature. These results suggest that hypothalamic substance P synthesized in the spinal ganglia is transported in the dorsal root toward their intraspinal axon terminals, where the substance is concentrated and serves as a neurotransmitter.
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PMID:Regional distribution of substance P in the spinal cord and nerve roots of the cat and the effect of dorsal root section. 16 61

Substance P has a powerful excitant action on spinal motoneurons of the newborn rat, and the action is specifically antagonized by Lioresal, which also readily blocks spinal reflexes involving primary afferent transmission. Substance P is highly concentrated in bovine and feline dorsal roots as well as in the dorsal part of the dorsal horn of cat spinal cord. There is evidence that substance P is synthesized in spinal ganglia, transported through the dorsal roots and stored in the axon terminals of primary afferent neurons. These and other results suggest that the undecapeptide substance P, or one of its shorter C-terminal analogues, functions as an excitatory transmitter of the primary afferent fibers.
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PMID:Substance P and primary afferent transmission. 19 49

1. The actions of microelectrophoretically administered substance P on Renshaw cells in pentobarbitone anaesthetized cats were investigated. 2. The effects on spontaneous and synaptic firing and interactions with a number of other agents including acetylcholine, acetyl-beta-methylcholine, acidic amino acids, morphine, dihydro-beta-erythroidine and strychnine were studied in attempts to elucidate the mechanism of action of substance P. 3. Substance P usually selectively depressed the excitation by ACh, and also reduced submaximal synaptically evoked discharges which activate nicotinic receptors, but failed to modify excitation caused either by acetyl-beta-methylcholine, which activates muscarinic receptors, or excitation caused by glutamate or homocysteate. Substance P also depressed excitation by morphine which acted via the nicotinic receptors. 4. The inhibitory effect was not blocked by strychinine and was considered to be unlikely to be due to interaction between the polypeptide and either glycine or GABA receptors. 5. On some cells substance P caused excitation which was blocked by dihydro-beta-erythroidine. Mixed excitatory-inhibitory effects were observed on some of these neurones. 6. The results are discussed in relation to the possibility that substance P could function as a synaptic inhibitory mediator with an unusual selectivity of action.
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PMID:Substance P and Renshaw cells: a new concept of inhibitory synaptic interactions. 20 46

Substance P produces analgesia when administered to mice in very small doses by the intraventricular route (1.25 to 5 nanograms per mouse). The analgesic effect can be blocked by naloxone. At higher doses (greater than 50 nanograms per mouse), this activity is lost. At these higher doses, however, substance P produced hyperalgesia when combined with naloxone and analgesia when combined with baclofen [beta-(4-chlorophenyl)-gamma-aminobutyric acid]. Substance P may have dual actions in brain, releasing endorphins at very low doses and directly exciting neuronal activity in nociceptive pathways at higher doses.
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PMID:Dual actions of substance P on nociception: possible role of endogenous opioids. 20 12

Effect of methionine-, leucine-enkephalin (met-, leu-enkephalin) and substance P on the transmission in mouse vas deferens was studied. Both met- and leu-enkephalin inhibited electrically induced contraction of vas deferens at 10(-8)-10(7) M, met-enkephalin being 1.4 times more active than leu-enkephalin. Nalorphine (10(-6) M) antagonized these effects. Substance P (10(-9)-10(-7) M) had no effect on the contraction. Met- and leu-enkephalin (10(-7)-10(-5) M) decreased the high potassium induced [3H]-norepinephrine release from vas deferens, while substance P (10(-6) M) significantly increased it. Nalorphine (10(-5) M) reversed the inhibitory effect of met-enkephalin. These results indicate that these peptides modify the transmission of sympathetic nerve in mouse vas deferens.
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PMID:Effect of enkephalin and substance P on sympathetic nerve transmission in mouse vas deferens. 20 50

The uptake kinetics of DL-[3H]-norepinephrine into synaptosomes from rat brain hypothalamus can be described as a two stage process with uptake constants of Km = 0.9 micron and Km = 0.06 micron, respectively. Substance P exerts an inhibiting influence on both uptakes. The possible importance of this inhibition for the regulation of noradrenergic transmission is discussed.
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PMID:[Inhibition of 3-H-noradrenalin uptake in synaptosomes by substance P]. 20 37

1. The mechanism of action of agonists that stimulate K release from the parotid gland was investigated by monitoring efflux of 86Rb from rat parotid slices. 2. As in previous studies, the 86Rb release was increased by agonists in a biphasic manner. An early, transient phase occurred that was independent of extracellular Ca. This was followed by a sustained (or slowly falling phase) that required extracellular Ca. 3. The agonists were investigated as to their additivity and to their sensitivity to inhibition by a number of putative Ca-antagonists. 4. When carbachol, epinephrine and Substance P were employed in supramaximal concentrations, no combination of agonists produced a summated 86Rb release response, despite the fact that the Ca concentration was submaximal. 5. The sustained phase of 86Rb release, which is dependent on extracellular Ca, was blocked by La, Ni, Co and neomycin; the transient phase was unaffected by these agents. 6. The local anaesthetics tetracaine and procaine inhibited both the transient and sustained phases of the responses to carbachol and phenylephrine; responses to Substance P and to the divalent cationophore, A23187, were largely refractory to this effect. 7. These results support the contention that, in the parotid, muscarinic, alpha-adrenergic and peptide receptors regulate the same Ca influx sites. 8. Also, these results suggest that La, Ni, Co and neomycin appear to antagonize the action of Ca by impeding inward movement of the cation through activated Ca influx sites. 9. Finally, the local anesthetics appear to inhibit, and therefore, serve to define, a transduction step between receptor occupation and channel activation. 10. In the case of the Substance P mechanism, it appears that the transduction mechanism must be qualitatively different to that for the muscarinic or alpha-adrenergic mechanisms.
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PMID:Control of calcium channels by membrane receptors in the rat parotid gland. 20 74


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