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)

1. The partition of substance P (SP) between buffer solutions (pH 1.6--7.8) and an organic, phospholipid (phosphatidyl serine, phosphatidyl ethanolamine, phosphatidyl inositol and phosphatidyl choline) containing phase (chloroform:methanol 2:1) was studied. 2. The binding of SP to phosphatidyl serine, phosphatidyl ethanolamine and phosphatidyl inositol was lowest at pH 2 and increased with pH. The binding to phosphatidyl choline was much smaller and less dependent on pH. 3. In contrast to the basic peptide SP (pI 10.5), physalaemin (pI 7.0) did not show any binding to phospholipids at any investigated pH value which underlines the importance of a basic group in the peptide for its binding. 4. The high affinity (KD = 0.1 microM) and capacity of 44 pmol SP/microgram phosphatidyl serine and 48 pmol SP/microgram phosphatidyl ethanolamine at pH 7.2 under conditions of saturation contrasted with the very low binding of SP to phosphatidyl inositol or phosphatidyl choline. Ionic bindings between the basic peptide and phosphatidyl serine or phosphatidyl ethanolamine are regarded to be predominant, although other binding forces cannot be excluded. 5. There was a concentration-dependent reduction in the binding of SP to phosphatidyl serine or phosphatidyl ethanolamine by Na+ and Ca2+, whereas K+ showed hardly any effect at physiological concentrations. 6. The model studies served to consider the possibilities of the binding of a basic peptide to lipid storage or receptor sites.
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PMID:Substance P: model studies of its binding to phospholipids. 3 6

The possibility that L-glutamate is the excitatory transmitter at the Drosophila larval neuromuscular junction and the ionic basis of its action on the muscle membrane are examined. 2. Iontophoretically applied L-glutamate causes muscle depolarization (L-glutamate potential) if and only if the L-glutamate pipette is within a few mum of the nerve ending. D-glutamate, substance P, ACh and GABA are ineffective. 3. Bath-applied L-glutamate produces similar changes in the time course and amplitude of miniature excitatory junctional potential (m.e.j.p.), excitatory junctional potential (e.j.p.) and the L-glutamate potential. 4. Neuromuscular transmission and excitation-contraction coupling are operative in a haemolymph-like solution containing 1 mM L-glutamate. 5. The reversal potentials of the e.j.p. and the L-glutamate potential are identical to each other, changing similarly with changes in the ionic compositions of the external medium (twelve solutions). 6. The ionic dependence of the reversal potentials is predicted from an extended constant-field equation using a ratio of sodium:potassium permeabilities of PNa/PK=1-3, and a ratio of magnesium:potassium permeabilities of PMg/PK=4-7. 7. It is concluded that L-glutamate is, or is an agonist of, the excitatory transmitter at certain Drosophila larval neuromuscular junctions.
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PMID:L-glutamate as an excitatory transmitter at the Drosophila larval neuromuscular junction. 18 87

The effects of various polypeptide enterohormones and the tachykinin secretogogue, physalaemin, on electrolyte transport by the main excretory duct of the mandibular gland of the rabbit were studied in vitro. Vasoactive intestinal peptide (VIP, 2 X 10(-11) mol 1(-1)) and gastric inhibitory polypeptide (GIP, 10(-11) mol 1(-1)) reduced nett Na+ movement from lumen to interstitium and VIP also reduced the transepithelial potential difference; the effective concentrations of the two hormones lay within the range of normal plasma concentrations. Gastrin (5 x 10(-7) mol 1(-1)) and synthetic secretin (2 x 10(-7) mol 1(-1)) had similar effects but only at concentrations well above the normal plasma levels. Caerulein, an analogue of the octapeptide of cholecystokinin, had no effect on duct function even at a concentration of 10(-6) mol 1(-1). The potent salivary secretogogue, physalaemin (4 x 10(-8) mol 1(-1)), which is an analogue of Substance P, a putative mammalian enterohormone and neurotransmitter substance, caused a marked increase in ductal Na transport (in rat as well as rabbit). It is concluded that VIP and GIP would normally play a role in determining salivary electrolyte composition and it is postulated that their action may be antagonized by a tachykinin such as Substance P.
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PMID:Modification of salivary duct electrolyte transport in rat and rabbit by physalaemin, VIP, GIP and other enterohormones. 56 44

Nine anesthetized dogs were provided with acute common duct fistulas after exclusion of the gallbladder. Synthetic Substance P was administered as caval infusions in a dosage of 0.5-20 ng x kg-1 x min-1, duration 10 min. The output of hepatic bile, sodium and amylase decreased during infusion by 40-52 per cent at the highest doses. After termination of infusion all 3 parameters increased by 19-60 per cent above the basal level. The biliary concentration of sodium was constant, while that of amylase increased during infusion. The responses were dose-related. The anticholeresis induced by substance P might be due to inhibition of the canalicular bile fraction, which presumably is mediated by active sodium transport and independent of bile salt excretion.
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PMID:Anticholeretic effect of substance P in anesthetized dogs. 64 72

Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. The correlation also exists during arterial infusion of angiotensin II, substance P and various vasodilators. During sodium depletion, the stimulation of the renin-angiotensin system causes increased drinking in rats and rabbits. The high angiotensin levels would stimulate kallikrein excretion. The excretion of water and dilution of urine are facilitated by the renal kallikrein-kinin system, even when antidiuretic hormone is high. This negative correlation between urinary osmolality and kallikrein excretion exists during arterial infusion of angiotensin or substance P and various vasodilators. During renal artery constriction, the kallikrein release per minute decreases, but over successive 10-minute periods, the kallikrein concentration in urine rises. This rise is correlated with some recovery in the clearance of rho-aminohippurate and inulin. Since kallikrein is released into renal lymph during saline infusion at a rate that correlates with its release into the urine, it is suggested that the renal kallikrein-kinin system protects the renal vasculature against the constricting action of the renin-angiotensin system. The decreased release of kallikrein (via the lymphatics into the circulation) during renal artery constriction, or decreased renal compliance, would potentiate the hypertensive effect of these procedures which cause increased renin release.
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PMID:The renal kallikrein-kinin system and the regulation of salt and water excretion. 76 62

Micropuncture and clearance techniques were used simultaneously to determine the effect of substance P on proximal tubular and overall renal function in anesthetized rats. This polypeptide, infused in saline at 50 pg/min into the abdominal aorta above the renal arteries, produced increases in urine flow, 2.7-3.7 mul/min.g kidney wt (P is less than 0.005); urinary sodium concentration, 32-61 meq/liter (P is less than 0.01); and sodium excretion, 89-223 neq/min (P is less than 0.005). Tubular fluid to plasma inulin concentration ratio measured in the last accessible proximal convolution fell from 2.21 to 1.80 (P is less than 0.001), and thus fractional reabsorption was reduced from 54 to 44% (P is less than 0.001). Absolute reabsorption by the proximal convoluted tubule was also reduced 15.5-12.5 nl/min (P is less than 0.025). In a control series of animals, saline alone infused at the same rate did not produce any statistically significant changes in the measured parameters over the same time period. The intrerenal mechanism responsible for the reduction in proximal reabsorption appears to be a tubular one since no consistent or significant changes were observed in kidney or single nephron glomerular filtration rate, renal plasma flow, or intrarenal hydrostatic pressures. No evidence was found to indicate redistribution of filtration rate, or plasma flow, or a reduction in filtration fraction.
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PMID:Effect of substance P on proximal tubular reabsorption in the rat. 93 56

Substance P (SP) binding protein of rat brain was solubilized by digitonin. The solubilized proteins were then purified by sequential gel filtration, concanavalin A lectin Sepharose, and SP-affinity chromatography. The calculated molecular weight of this purified SP binding protein was 76-74 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The rabbits were immunized with the purified protein and resulting polyclonal anti-sera were tested. The immune serum significantly inhibited [3H]SP binding to the 3-[(3-cholamidopropyl)dimethylammonio]-1-propane sulfonate solubilized membrane fractions from rat brain, whereas pre-bleed antiserum failed to inhibit the binding. This polyclonal antibody also inhibited the activity of 45Ca influx into astroglioma cells stimulated by SP, but does not inhibit that stimulated by histamine. Furthermore, this polyclonal antibody recognized the 76-74 kDa band as assessed by Western blotting. These data strongly suggest that this polyclonal antibody could recognize a part of the natural SP receptor site.
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PMID:Isolation of substance P binding protein from rat brain. 127 54

Whole-cell recordings were made from neurons of the rat locus coeruleus in a tissue slice removed from rat brain. Substance P caused an inward current in cells voltage-clamped at -60 mV. The effect of substance P was concentration-dependent (30 nM-3 microM) and was mimicked by similar concentrations of substance K and neuromedin K. The inward current resulted predominantly from an increase in membrane cation conductance; in potassium-free solutions it reversed polarity at about 12 mV. Substance P also reduced the conductance of an inwardly rectifying potassium current; this action was studied with low external sodium concentration. It is concluded that substance P excites rat locus coeruleus neurons by activating an intracellular transduction pathway leading to both cation conductance increase and potassium conductance decrease.
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PMID:Substance P opens cation channels and closes potassium channels in rat locus coeruleus neurons. 127 60

An active gelatinase has been purified from the conditioned medium of granulation tissue culture formed by carrageenin injection in rats. The purified gelatinase gave a single band corresponding to a M(r) of 57 kDa on both sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and SDS-gelatin PAGE. The granulation tissue-derived gelatinase selectively cleaved the Gln6-Phe7 bond of substance P (SP) with a Km of 0.17 mM and a Vmax of 0.027 nmol SP7-11/min/micrograms protein, resulting in the generation of biologically inactive fragments, SP1-6 and SP7-11. Our data suggest that the gelatinase produced by granulation tissue participates in the inactivation of SP in the inflammatory site.
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PMID:Inactivation of substance P by granulation tissue-derived gelatinase. 128 Apr 34

The effect of synthetic substance P (SP), infused intravenously in doses of 0.5, 1 or 1.5 pmol/kg-1/min-1 over 60 min on ACTH/cortisol secretion was evaluated in 7 healthy men. SP tests and a control test with normal saline were randomly performed at weekly intervals. During tests, SP infusion did not produce untoward side effects or changes in blood pressure. Plasma ACTH and cortisol levels were not modified when normal saline or the lowest dose of SP were infused, whereas they were significantly increased in a dose-dependent fashion when higher amounts of SP were administered. Further studies were performed in another 7 healthy men to test the possible influence of GABAergic neurotransmission on the ACTH/cortisol response to SP. For this purpose, subjects were tested with SP (1.5 pmol/kg-1/min-1) alone and on a different occasion with SP after pretreatment with the GABAergic agent sodium valproate (200 mg 16, 8 and 1 h before the SP test). Again, the administration of SP induced a significant increase in plasma ACTH and cortisol levels. The pretreatment with sodium valproate completely abolished both ACTH and cortisol responses to SP. These data demonstrate for the first time in humans that the systemic infusion of SP stimulates ACTH/cortisol secretion, suggesting the involvement of a GABAergic mechanism in the regulation of the action of SP.
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PMID:Stimulation of ACTH/cortisol by intravenously infused substance P in normal men: inhibition by sodium valproate. 128 18


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