Storage Properties of Rat Mast Cell Granules In vitro

Bergendorff, Anders; Uvnäs, Börje

doi:10.1111/j.1748-1716.1973.tb05383.x

Cited by 44 publications

(13 citation statements)

References 15 publications

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“…Thus, when granular material is not set free from the cells, 45Ca uptake still proceeds, but is reduced. It is likely that this reduction of 45Ca uptake in the presence of metabolic inhibitors is due to the loss of Ca binding caps ity presented by the released granular material which is known to have a high affinity for calcium (Bergendorff & Uvnas, 1973). Nevertheless, the conclusion is that about two thirds of the 45Ca uptake induced by antigen stimulation, or for that matter by ionophore, is independent of the process of granule extrusion.…”

Section: Discussioncontrasting

confidence: 38%

The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells

Foreman¹,

Hallett²,

Mongar³

1977

The Journal of Physiology

279

135

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SUNMMARY1. Unstimulated mast cells from the peritoneal cavity of the rat take up 45Ca: the initial phase of rapid uptake being complete after 1 min incubation of the cells with the isotope. Stimulation of the mast cells with an antigen-antibody reaction, dextran or concanavalin A induces an increase in the uptake of45Ca which is accompanied by a release of granular material: this increase in 45Ca uptake is also complete in 1 min. The majority of the stimulated 45Ca uptake cannot be explained in terms of binding of Ca to released granular material, or to an enlargement in either the extracellular compartment or the cell surface area.2. The magnitude of the increase in 45Ca uptake caused by stimulating the mast cells increases when the degree of histamine secretion increases.3. The increased 45Ca uptake induced by stimulation of the mast cells and the degree of histamine secretion are both dependent on extracellular H ion concentration. Changes of pH cause similar changes in 45Ca uptake and secretion with maxima at pH 7-5. 4. Two thirds of the 4"Ca uptake induced by an antigen-antibody reaction or by the Ca ionophore A 23187 is unaffected by inhibiting glycolysis and oxidative phosphorylation. Histamine secretion on the other hand is practically abolished by this metabolic inhibition. Thus, 45Ca uptake proceeds in the absence of the discharge of granules.5. Dibutyryl cyclic AMP or theophylline inhibit both the increase in 45Ca uptake and the histamine secretion caused by stimulating mast cells with an antigen-antibody reaction. Cyclic AMP, cyclic GMP and dibutyryl cyclic GMP have no effect on uptake or secretion.6. The Ca ionophore, A 23187, induces uptake of 45Ca and histamine secretion, neither effect being inhibited by either dibutyryl cyclic AMP or theophylline.7. Phosphatidyl seine increases both 45Ca uptake and the histamine release induced by an antigen-antibody reaction, dextran or concanavalin A.7-2

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Section: Discussioncontrasting

confidence: 38%

The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells

Foreman¹,

Hallett²,

Mongar³

1977

The Journal of Physiology

279

135

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“…These findings together with the observation of identical elimination rates of the two amines (see be low) thus indicate that they occupy identical storage sites in mast cell granules, confirming the results of binding studies in vitro on isolated mast cell granules [3], Our results further show that the binding sites for amines are almost fully saturated under normal con ditions in vivo. These considerations would seem to justify the use of 5-HT as a probe for histamine in studies on the biology of the rat mast cell.…”

Section: Discussionsupporting

confidence: 78%

Storage and Turnover of Histamine, 5-Hydroxytryptamine and Heparin in Rat Peritoneal Mast Cells in vivo

Wingren

Wasteson

Enerbäck

1983

Int Arch Allergy Immunol

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The biogenic amines and heparin of rat peritoneal mast cells were labelled in vivo by the injection of amine precursors (³H-histidine and ³H-5-hydroxytryptophan) and ³⁵S-sodium sulfate. Uptake of label was rapid, probably reflecting the synthesis of new granule material, but the elimination was slow. Half-lives of radiolabelled histamine (23 days) and 5-hydroxytryptamine (5-HT; 25 days) did not differ statistically from that of heparin (35 days). The slow elimination rates suggest that mast cell secretion is of little biological significance under normal conditions but are well compatible with the idea that mast cell function is related to secretion evoked by appropriate immunological stimuli. It further permitted an analysis of the amine storage by repeated injections of unlabelled 5-HT. A 15-fold increase in 5-HT content was obtained while the total amine content remained constant. The uptake of 5-HT was balanced by a reduction of histamine in a molar 1:1 ratio. A displacement of histamine by 5-HT was further indicated by increased elimination rate of radiolabelled histamine in response to 5-HT injections. The results support previous binding studies in vitro and indicate that histamine and 5-HT are bound to identical storage sites in the mast cell granules.

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“…Such a mechanism could account for the central observation that if Ca-rich vesicles are preferentially secreted (9), they must lose Ca and gain Na prior to secretory dispersion. The conversion from Ca-rich vesicles to Na-rich vesicles can be explained by Donnan equilibrium-driven Na ϩ uptake followed by competition between these ions for the anionic sites of the vesicular matrix (33,34).…”

Section: Discussionmentioning

confidence: 99%

Stimulus–secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium?

Thirion

Jd²,

Nb³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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It is generally accepted that Ca is essentially involved in regulated secretion, but the role of this cation, as well as others such as Na, is not well understood. An illustrative example occurs in neurohypophysial secretion, where an experimentally induced increase in the cytosolic concentration of Na ؉ can induce continuous neuropeptide release. In contrast, an increase in cytosolic Ca 2؉ will have only a transient stimulatory effect. The secretion-promoting targets for Ca 2؉ are not known; they may be cytosolic, as is usually assumed, but they may also be intravesicular, especially in view of evidence that Ca-rich secretory vesicles are preferentially secreted. In the present work, we have investigated the movements of these cations into and out of secretory vesicles during stimulus-secretion coupling. Isolated rat neurohypophysial nerve endings were stimulated by potassium (55 mM) depolarization, and at 6 min (peak secretion) and 20 min after the onset of stimulation, the elemental content of individual secretory vesicles was measured by quantitative x-ray microanalysis. A depolarization-induced transient increase in intravesicular Na ؉ concentration was found to coincide with the onset of secretion. Moreover, only a predicted small fraction of peripheral vesicles-presumably the docked ones-were Na ؉ -loaded. The low sulfur concentration of Na ؉ -rich vesicles most likely resulted from vesicle swelling. The results suggest that high intravesicular Na ؉ concentrations in docked vesicles, occurring by Na ؉ ͞Ca 2؉ exchange or by transient fusion pore opening, is a proximal event in exocytosis. Ca 2ϩplays an essential role in several stimulatory, and perhaps also inhibitory, steps of regulated exocytosis but, despite much recent progress, its precise targets are still largely a matter of debate (1-3). In neurohypophysial secretion particularly, it is clear that Ca 2ϩ cannot be the ultimate and sufficient trigger for neurosecretion, because the obligatory depolarizationinduced increase in cytosolic Ca 2ϩ concentration stimulates release for only a few minutes (4, 5), even when depolarization is maintained. This behavior contrasts with the known but mechanistically obscure secretagogue effect of Na ϩ (6-8), wherein an artificially induced increase in cytosolic Na ϩ concentration can induce a sustained and continuous secretion (8). In previous work on neurohypophysial nerve endings, one of our laboratories reported that the Ca content of the secretory vesicles increased upon secretory stimulation, and that Ca-rich vesicles accumulated when secretion was blocked (9), suggesting a role of intravesicular ion concentration in the secretory mechanism. This hypothesis is further supported by observation that in insulin-secreting cells, Ca 2ϩ depletion from secretory granules inhibits exocytosis (10). Because the swelling of some granule matrices is inhibited by Ca 2ϩ and promoted by Na ϩ (11, 12), we have investigated in isolated and stimulated rat neurohypophysial nerve endings possible changes in the concentra...

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Storage Properties of Rat Mast Cell Granules In vitro

Cited by 44 publications

References 15 publications

The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells

The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells

Storage and Turnover of Histamine, 5-Hydroxytryptamine and Heparin in Rat Peritoneal Mast Cells in vivo

Stimulus–secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium?

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Storage Properties of Rat Mast Cell Granules In vitro

Cited by 44 publications

References 15 publications

The relationship between histamine secretion and 45calcium‐uptake by mast cells

The relationship between histamine secretion and 45calcium‐uptake by mast cells

Storage and Turnover of Histamine, 5-Hydroxytryptamine and Heparin in Rat Peritoneal Mast Cells in vivo

Stimulus–secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium?

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The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells

The relationship between histamine secretion and ⁴⁵calcium‐uptake by mast cells