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)

Intracellular recordings of membrane potential and membrane currents were made from neurones in the submucous plexus of the guinea-pig caecum in vitro. Fast and slow excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were recorded from the majority of neurones following focal stimulation of presynaptic fibres in the plexus. The slow inhibitory postsynaptic potential was associated with an increase in membrane conductance and reversed its polarity at -90 mV; it was reversibly blocked by yohimbine. The slow excitatory postsynaptic potential and its underlying current was associated with a decrease in membrane conductance. Two kinds of voltage-dependence both of the slow excitatory postsynaptic potential and current were observed; in 80% of cells, the excitatory postsynaptic potential and current became smaller with membrane hyperpolarization and reversed polarity at -90 mV (reversing type) but in 20% of cells both the excitatory postsynaptic potential and current simply disappeared when the membrane potential reached -70 mV (non-reversing type). The effects of acetylcholine, adenosine 5'-triphosphate, bombesin, 5-hydroxytryptamine, neurotensin, noradrenaline, substance P and vasoactive intestinal polypeptide were examined. The only substance which mimicked the slow inhibitory postsynaptic potential was noradrenaline; brief applications of noradrenaline caused hyperpolarizations which had the same time-course, reversal potential and sensitivity to yohimbine as the slow inhibitory postsynaptic potential. The non-reversing type of slow excitatory postsynaptic potential was mimicked only by adenosine 5'-triphosphate. The reversing type of slow excitatory postsynaptic potential was mimicked by bombesin, neurotensin, substance P and vasoactive intestinal polypeptide. 5-Hydroxytryptamine and vasoactive intestinal polypeptide (in some neurones) caused a depolarization with an increase in membrane conductance. All three synaptic potentials were reversibly depressed by superfusion of noradrenaline but noradrenaline did not affect the potential changes evoked by brief application of exogenous acetylcholine or substance P. It is concluded that, in guinea-pig submucous plexus neurones, the slow inhibitory postsynaptic potential is mediated by noradrenaline and results from a potassium conductance increase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Slow postsynaptic potentials in neurones of submucous plexus of guinea-pig caecum and their mimicry by noradrenaline and various peptides. 241 86

Superfusion of slices of the dorsal half of rat spinal cord in vitro with 10 microM capsaicin or 60 mM potassium lead to the simultaneous release of substance P (SP)-, neurokinin A (NKA)- and calcitonin gene-related peptide (CGRP)-like immunoreactivities (LI). The ratio between capsaicin-stimulated and basal release was higher for CGRP-LI than for SP-LI, indicating that relatively more CGRP is released from sensory nerves, whereas SP is not only released from afferent neurons. High-performance liquid chromatography of NKA-LI revealed several immunoreactive components. One major peak had the retention time of synthetic NKA. A second peak eluted close to the position of synthetic eledoisin. In conclusion, capsaicin releases several bioactive peptides from sensory neurons which may mediate the acute algetic effect of chemical irritants.
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PMID:Simultaneous release of several tachykinins and calcitonin gene-related peptide from rat spinal cord slices. 241 7

The effects of the dihydropyridine calcium channel entry blockers nifedipine and nilvadipine on colonic contractions were determined in vitro and in vivo. In circular muscle strips prepared from the canine proximal colon, cumulative concentration-response curves were generated to potassium chloride (KCl), acetylcholine (ACh) and substance P, and the effects of electrical field stimulation were determined. Responses to KCl and ACh were examined in circular muscle strips prepared from the monkey proximal and distal colon. Nifedipine (10(-8) - 10(-6) M) significantly decreased KCl-induced contractions, whereas equimolar concentrations of nilvadipine were less effective at modifying these responses. Both calcium channel entry blockers produced similar significant decreases in ACh, substance P and electrical field stimulation contractions. In anesthetized dogs, strain gauge force transducers were oriented to record proximal colonic circular muscle contractions. Colonic contractions to i.a. infusions of ACh, cholecystokinin-(26-33) and substance P were produced in a small segment of the proximal colon. Nifedipine and nilvadipine (200 micrograms/kg i.v.) significantly decreased maximal ACh contractions. Nilvadipine also decreased maximum cholecystokinin-(26-33) and substance P contractions. Both calcium channel entry blockers decreased systolic and diastolic blood pressure significantly at 100 micrograms/kg i.v. These results indicate that nifedipine and nilvadipine are equieffective at reducing colonic contractile activity to a variety of colonic stimulants and illustrate the importance of extracellular calcium in the mediation of colonic motility
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PMID:Effects of calcium channel entry blockers, nifedipine and nilvadipine, on colonic motor activity. 242 Sep 71

This study was initiated to determine if raised (carcinoid) plasma concentrations of substance P induced jejunal secretion of water and electrolytes. Five dogs had isolated and cannulated 25 cm jejunal segments perfused at 2 ml/min with a neutral, isotonic perfusate. Saline, 1.0 ml, was infused intravenously during basal and recovery periods, while substance P was administered intravenously at 75 ng/kg/min (55 pmol/kg/min) during the four 15 minute experimental periods. Infusion increased plasma SP concentrations from basal (5.8 +/- 1.3 pg/ml) to a mean plateau level of 121.2 +/- 25.2 pg/ml (mean +/- SEM). During SP infusion, intestinal secretion of water, Na+, and Cl- were documented (H2O basal +102 +/- 60 to SP -275 +/- 60; microliter/min; Na+ basal +19.8 +/- 7.2 to SP -23.2 +/- 7.5 microEq/min; Cl- basal 21.7 +/- 7.5 to SP -16.5 +/- 5.6 microEq/min). Under basal conditions, there was minimal secretion of potassium (-0.264 +/- 0.282 microEq/min); during SP infusion, K+ flux was altered to significant secretion (-1.784 +/- 0.271 microEq/min). Serum concentrations of Na and Cl were unchanged during SP infusion, but serum potassium concentrations fell from 4.64 +/- 0.12 to 3.85 +/- 0.40 mEq/l. The data demonstrate that substance P at levels noted in the carcinoid syndrome induces significant jejunal secretion of water and electrolytes in the dog.
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PMID:Substance P-induced intestinal secretion of water and electrolytes. 242 93

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 effect of temperature on the substance P-induced contraction of the isolated tracheal strip-chain preparation from the golden hamster has been examined. A decrease of bath temperature from 37 to 20 degrees C augmented the contractile response of the trachea caused by substance P. Similar cooling-induced augmentation was observed in the contractile responses to caffeine and carbachol, but not to potassium chloride. The increased responsiveness with lowered temperature of the trachea to substance P may be due to the acceleration of Ca2+ release from an intracellular storage site.
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PMID:Cooling-induced augmentation of the contractile response of the golden hamster tracheal muscle to substance P in-vitro. 242 77

The concentration of potassium ions in a superfusate of rat parotid gland fragment was continuously monitored by potassium selective electrodes to assess the rate of potassium secretion by the gland. The potassium concentration determined from the electrode readings agreed well with values obtained by atomic absorption (r = 0.99). The detection limit for changes in potassium concentration was approximated to 50 microM K+. When medium was recirculated over the gland fragments it was possible to detect even small changes in the rate of potassium efflux. Thus, increases in potassium secretion following administration of substance P (SP) down to 0.1 nM and carbacholine 10 nM was registered. When the buffer medium was passed only once over the gland fragments it was possible to reproducibly study the time course of potassium secretion. However, with this system higher doses of secretagogues were required for detection of potassium efflux, since the potassium secernated was diluted by the perifused buffer. Following SP (0.01 or 0.1 microM) or carbacholine (1 or 10 microM) a peak of potassium secretion was registered during the first 8-10 min, which was followed by a steady low rate. The metabolic state of the gland fragments, as determined by the ratio of adenine nucleotides, was similar to that found in vivo even after an experiment of several hours' duration. However, the viable part of the glandular tissue, calculated as the content of adenine nucleotides per mg protein, was decreased to approximately 30% compared to the intact gland in situ.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Continuous monitoring of potassium efflux from rat parotid gland fragments by potassium selective electrodes. 242 70

We studied whether morphine, norepinephrine (NE), 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA) inhibit the potassium-stimulated release of substance P (SP) from rat spinal cord slices. Male Sprague-Dawley rats were decapitated and a 2-cm segment of lumbosacral spinal cord was removed, chopped into 0.5 X 0.5 mm pieces, weighed, placed in a perfusion chamber and perfused at 37 degrees C with a modified Krebs bicarbonate buffer. Perfusate was collected, lyophilized, then assayed for SP using radioimmunoassay. Exposure of spinal cord tissue to 50 mM KCl for 8 min produced a calcium-dependent increase in the release of SP from a basal level of approximately 0.1 pg/mg tissue/min to 0.3 pg/mg tissue/min. Morphine and NE at concentrations of 10(-4) and 10(-5) M did not alter basal release but caused a significant reduction in the potassium-stimulated release of SP. Naloxone (10(-5) M) and phentolamine (10(-5) M) did not affect SP release but attenuated the effects of morphine and NE, respectively. Naloxone did not antagonize the inhibition of release produced by NE nor did phentolamine block the effect of morphine, suggesting that the actions of the agonists are independent. In contrast, 5-HT and GABA at concentrations of 10(-4) M and 10(-5) M did not significantly alter the basal or potassium-stimulated release of SP. These results demonstrate a differential regulation of SP release in the spinal cord and support the hypothesis that morphine and NE may modify nociception, in part, by inhibiting the release of SP in the spinal cord.
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PMID:Morphine and norepinephrine but not 5-hydroxytryptamine and gamma-aminobutyric acid inhibit the potassium-stimulated release of substance P from rat spinal cord slices. 242 94

The release of tachykinins from isolated slice preparations of the guinea-pig spinal cord and ureter was studied in vitro. Capsaicin (10 microM) caused release of substance P, neurokinin A and an eledoisin-like component from both the spinal cord and ureter. The release of tachykinins induced by capsaicin or potassium (60 mM) was calcium dependent. No detectable release of neurokinin B or neuropeptide K, an N-terminally extended form of neurokinin A, was induced by capsaicin. No detectable release of tachykinins could be demonstrated after exposure to agents which are known to activate C-fibre afferents, such as histamine, bradykinin, serotonin, prostaglandins E1, E2 or acetylcholine. Protein extravasation in the ureter, as determined by the Evans Blue extravasation technique was used as a functional correlate to the tachykinin release. Protein extravasation was induced in vivo by local intraluminal injections of capsaicin at several hundred-fold lower concentrations than those required to induce a detectable release of tachykinins in vitro. The difference may, however, partly depend on the experimental conditions and the detection limit of the tachykinin assay used. The protein extravasation response to capsaicin was absent after systemic capsaicin pretreatment, which causes a marked depletion of tachykinins in the ureter. In conclusion, capsaicin evokes release of several tachykinins from both central and peripheral endings of primary afferent neurons. The peptides released from sensory nerves in the periphery may induce effects such as protein extravasation and smooth muscle contraction.
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PMID:Capsaicin induced release of multiple tachykinins (substance P, neurokinin A and eledoisin-like material) from guinea-pig spinal cord and ureter. 243 50

The effect of substance P (sP) on mammalian skeletal myoneural transmission was studied employing innervated and denervated isolated rat diaphragm preparations. sP at a concentration of 3.7 nM facilitated the indirect twitch responses of the rat diaphragm and antagonised the paralytic effect of d-tubocurarine (d-Tc). sP failed to affect the direct twitch responses as well as the contractures induced by acetylcholine (ACh) and potassium chloride (KCl) in the denervated diaphragm. The amount of ACh released into the bathing medium in response to tetanic stimulation of the phrenic nerve was doubled in presence of sP. The study illustrates a presynaptic facilitatory involvement of sP on mammalian myoneural transmission.
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PMID:Possible functional role of substance P on the mammalian motor nerve terminals. 243 78


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