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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated rat peritoneal mast cells released histamine on superfusion with isotonic salt solutions or isotonic deionized sucrose. The histamine release followed the kinetics of cation exchange characteristic of the release from similarly superfused isolated mast cell granules and histamine charged carboxylic resin IRC-50. The histamine release was accompanied by an efflux of potassium and ascribed to an endogenous cation exchange K+ in equilibrium with Hi+ occurring on the passage of outflowing potassium ions over histamine storing granules.
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PMID:Do superfused mast cells release histamine by endogenous cation exchange with potassium ions? 244 Feb 56

The transfer of rat peritoneal mast cells from balanced salt solution to calcium-free buffer led to a time-dependent decrease in their response to compound 48/80 and to ionophore A23187. The concomittant absence of potassium from the calcium-free buffer enabled the mast cells to retain their secretory response. The increase in potassium level, with a parallel decrease in sodium to maintain osmolarity, led to a slight potentiation of the response to 48/80 and to a large but transient potentiation of the response to A23187. Mast cells can be considered nonexcitable. The apparent dependency upon extracellular calcium of mast cell secretory responses might be related to the presumed tight equilibrium between endoplasmic reticulum calcium stores and extracellular calcium. The control of this equilibrium by transmembrane gradients of monovalent ions is proposed.
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PMID:Preservation of the secretory response of peritoneal mast cells in the absence of extracellular calcium. 244 99

Dendrotoxin and mast cell degranulating peptide are highly potent convulsant polypeptides from mamba snake and bee venoms, respectively. Electrophysiological techniques and binding assays were used to study their interaction with fast-activating, voltage-dependent potassium channels in rat neurons. Intracellular recordings in sensory ganglion cells showed that mast cell degranulating peptide blocks the same slowly inactivating potassium current as dendrotoxin but with lower potency, the respective IC50 values in sensory A neurons of nodose ganglion being 2.1 nM and 37 nM. In contrast, the transient potassium current (IA) in superior cervical ganglion neurons was unaffected by either toxin, highlighting the heterogeneity of these potassium channels and the selective action of the toxins. Using biologically active 125I-labelled derivatives of dendrotoxin and beta-bungarotoxin (a related snake protein), the binding of mast cell degranulating peptide to two subtypes of high-affinity acceptors in rat cerebrocortical synaptosomal preparations was examined. Mast cell degranulating peptide antagonized the specific binding of both radioiodinated toxins to each of the acceptor species, in the membrane-bound state; additionally, [125I]dendrotoxin binding in detergent-solubilized extracts was, likewise, blocked by mast cell degranulating peptide. Notably, the observed inhibitory constants (KI) for mast cell degranulating peptide were appreciably larger than for dendrotoxin, consistent with their different efficacies in blocking the potassium conductances. It is concluded that the specific interaction of this apian polypeptide with dendrotoxin acceptors must underlie its selective action on potassium conductances, emphasizing a functional relationship between these membrane acceptors and the potassium channel variants, sensitive to both dendrotoxin and mast cell degranulating peptide.
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PMID:Mast cell degranulating peptide and dendrotoxin selectively inhibit a fast-activating potassium current and bind to common neuronal proteins. 244 37

Incubation of rat peritoneal mast cells with substance P resulted in the transient stimulation of phosphoinositol breakdown and histamine secretion through an exocytotic process. These effects were inhibited markedly by a prior 2-hr exposure of the cells to pertussis toxin. Pertussis toxin also inhibited exocytosis induced by substance P, mastoparan and compound 48/80, but did not modify the secretory effect of the ionophore A23187. The transfer of rat peritoneal mast cells from balanced salt solution to calcium-free buffer led to a similar time-dependent decrease in their response to substance P and mastoparan. The concomitant absence of potassium from the calcium-free buffer enabled the mast cells to retain their secretory response. These data demonstrate identical dependency for calcium and monovalent ions of the secretory process elicited by substance P, mastoparan and compound 48/80. Pretreatment of mast cells with neuraminidase decreased the secretagogic effect of substance P, mastoparan and compound 48/80 without modifying the efficiency of the ionophore A23187. Thus, sialic acid residues might be involved in the initial binding of peptides and compound 48/80 to mast cells, which activate a pertussis toxin-sensitive G-protein and allows the increase in phospholipase C activity to induce exocytosis. This sequence of events might characterize the physiological pathway of mast cell activation by peptides, without necessarily requiring selective membrane receptors.
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PMID:Activation of rat peritoneal mast cells by substance P and mastoparan. 247 89

The mechanism(s) of adverse reactions to sulfites remains unclear. To determine whether mast cell degranulation is involved in sulfite sensitivity, we performed single-blind, placebo-controlled oral aqueous challenges with potassium metabisulfite in 13 patients with histories suggestive of sulfite sensitivity. Ten patients were also skin tested with potassium metabisulfite at 10 mg/mL and all had negative reactions. Serum samples were obtained from all the patients before the challenge and for 180 minutes after the challenge. The samples were tested for the presence of neutrophil chemotactic factor of anaphylaxis, using both a 51chromium microchamber chemotaxis assay and a leukocyte polarization technique. Six of 13 patients had positive challenges as defined by a fall equal to or greater than 20% in their forced expiratory volume in one second. No significant increase in neutrophil chemotactic factor activity was detected in the postchallenge serum samples from patients who experienced positive or negative challenges. We conclude that sensitivity to aqueous metabisulfite is not associated with mast cell degranulation in metabisulfite skin test-negative patients.
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PMID:Studies of neutrophil chemotactic factor of anaphylaxis in metabisulfite sensitivity. 291 98

An inhibitor of sodium-potassium-ATPase has been partially purified from the culture medium obtained from hypothalamic cells maintained in a capillary membrane perfusion system, and some of the properties of this inhibitory factor have been investigated. Gel filtration (Sephadex G-25 Superfine) of heat-treated medium (80 degrees C for 10 min) resulted in elution of inhibitory activity in the post-salt fraction. These fractions inhibited active (i.e. sodium-potassium-ATPase-mediated) sodium transport in intact human erythrocytes, displaced [3H]ouabain from its binding site, and directly inhibited canine kidney sodium-potassium-ATPase as measured by NADH oxidation. High-performance liquid chromatography (on Hypersil ODS) of these fractions after desalting yielded one region which showed inhibitory activity on all three assays. Inhibition of sodium-potassium-ATPase was dose-related and filtered through an Amicon UM10 membrane. Incubation of this material with dispase, carboxypeptidase A, chymotrypsin, and prolidase destroyed inhibitory activity, whereas trypsin and leucine aminopeptidase were ineffective. These studies show that hypothalamic neurones release a low molecular weight heat-stable peptide which inhibits active sodium transport, ouabain binding, and sodium-potassium-ATPase.
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PMID:Characterization and partial purification of the sodium-potassium-ATPase inhibitor released from cultured rat hypothalamic cells. 299 73

1. Using a previously established method of isolating an active-sodium-transport inhibitor (ASTI) from hypothalamic cell culture medium, the inhibitor was isolated and partially purified from sequential passages through Sephadex G-25 and h.p.l.c., and its effects on de-endothelialized rabbit aortic strips were investigated. 2. ASTI caused a cumulative concentration-dependent increase in tension which reversed slowly after wash, and the wash showed an identical effect on fresh strips. 3. Ouabain, used as a control, also caused a concentration-dependent increase in tension which reached a plateau at a concentration of 10 mmol/l. Both ouabain and ASTI caused a significant potentiation of the vasoconstrictor effect of noradrenaline at concentrations of 1 nmol/l-0.1 mmol/l. 4. Both ASTI and ouabain caused a significantly greater (P less than 0.01) calcium retention than control medium in aortic strips. 5. Incubation of ASTI with prolidase, chymotrypsin and carboxypeptidase A destroyed the vasoconstrictor effects as well as its inhibitory effects on sodium, potassium-dependent adenosine triphosphatase and sodium efflux from erythrocytes, but leucine aminopeptidase was ineffective. 6. These studies suggest that hypothalamic cells in culture release a peptidic inhibitor of active sodium transport which increases vascular reactivity, potentiates vasoconstrictor effects of noradrenaline and causes calcium retention.
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PMID:Calcium retention and increased vascular reactivity caused by a hypothalamic sodium transport inhibitor. 340 35

At 4 h after the intraperitoneal administration of kainic acid in a dose of 12 mg/kg, Evans blue extravasation was observed preferentially in the thalamus, accompanied by increases in the water and sodium contents and by a decrease in the potassium content. Subcutaneous pretreatment with a histamine H2-receptor blocking agent, ranitidine, in a dose of 5 mg/kg given 2 h before and at the time of kainic acid injection, partially decreased the edema formation in the thalamus. It is assumed that repetitive discharges evoked by the kainic acid result in the thalamus in an excessive release of histamine from internal (mast cell and neuronal) sources and that this leads to the activation of H2-receptor-coupled adenylate cyclase in the brain microvessels and to the induction of brain edema.
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PMID:Histamine H2-receptors participate in the formation of brain edema induced by kainic acid in rat thalamus. 364 81

Erabutoxin c, a minor neurotoxic component of the venom of a sea snake Laticauda semifasciata, was isolated in pure form by repeated column chromatography on CM-cellulose columns. The toxin was crystallizable and monodisperse in rechromatography, disc electrophoresis and isoelectric focusing (isoelectric point, pH9.23-9.25). The molecular weight of the toxin, as estimated by gel filtration, was 7000. The toxin showed the same lethal activity to mice (0.13mug/g body wt., intramuscular injection) and the same effect on isolated frog muscle as erabutoxins a and b, the main toxic components of the venom. The toxin inhibited the acetylcholine contracture but not the potassium chloride contracture of muscle. Erabutoxin c consisted of 62 amino acid residues, containing one fewer lysine and one more histidine than erabutoxin a and one fewer lysine and one more aspartic acid (or asparagine) than erabutoxin b. Erabutoxin c was reduced, S-carboxymethylated and hydrolysed with trypsin. The only fragment different from the corresponding fragments from erabutoxin b was hydrolysed further with pepsin. One of the peptic fragments, which was assumed to have the aspartic acid (or asparagine) residue in question at the C-terminal end, was treated with carboxypeptidase A. The C-terminal residue was found to be an asparagine. It was therefore concluded that erabutoxin c was [51-asparagine]-erabutoxin b.
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PMID:The isolation, properties and amino acid sequence of erabutoxin c, a minor neurotoxic component of the venom of a sea snake Katicauda semifasciata. 466 80

The effect of various fluorides as to their ability to activate mast cells to subsequent secretory action of calcium have been investigated. The mechanism of action of both potassium and lithium fluoride conformed to a secretory process by being dependent on calcium and cellular metabolic energy. On the other hand, the action of ammonium fluoride seemed to be cytotoxic. Among fluorides tested, potassium fluoride was shown to be the most potent agent. The potency of mast cell activatory action of fluorides was parallel to their dissociation constants.
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PMID:The action of various fluorides on rat mast cells. A comparative study. 616 44


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