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1. The release of 45calcium from prelabelled pancreatic islets is rapidly and almost totally inhibited by lanthanum. 2. Glucose provokes an intitial fall followed by a secondary rise in 45calcium efflux. The latter rise occurs concomitantly with insulin release. Its magnitude is reduced whenever the secretory response to glucose is inhibited, e.g. in the absence of extracellular calcium, presence of Verapamil, or at high magnesium concentration. 3. However, under suitable conditions, the glucose-induced secondary rise in 45calcium efflux is not totally suppressed whilst insulin release is totally abolished. 4. Inversely, when calcium is replaced by barium in the perifusate, glucose increases insulin output without causing any obvious secondary rise in 45calcium efflux. 5. It is concluded that this secondary rise, which originates from a lanthanum-nondisplaceable calcium pool, does not correspond solely to an exocytotic release of 45calcium. It could represent, in part at least, a displacement of 45calcium from cellular sites and reflect a glucose-induced increase in the rate of calcium entry in islet cells.
Decanoyl-, palmitoyl-, and oleoyl-lysophosphatidic acid (LPA) were studied for their effects on platelet aggregation and intracellular calcium flux. Palmitoyl-LPA and oleoyl-LPA both caused a concentration-dependent aggregation of human blood platelets at concentrations of 12--300 microM. Aggregation by adenosine diphosphate (ADP) was enhanced at slightly lower concentrations. First-wave aggregation induced by these LPAs was not blocked by aspirin, indomethacin, or heparin, suggesting similarities to ADP aggregation. However, in washed platelets with a high calcium concentration, no serotonin secretion was observed, even though full aggregation occurred, suggesting that aggregation was not due to released ADP. This concept was supported by studies of platelets deficient in the storage pool of ADP and serotonin, which had a normal first-wave aggregation response to palmitoyl-LPA. Aggregation induced by palmitoyl LPA was inhibited by prostaglandin E1 (PGE1), theophylline, and ethylenediaminotetraacetate (EDTA), though in the presence of EDTA shape change occurred. Aggregation stimulated by palmitoyl-LPA or oleoyl-LPA was characterized by changes in the shape of the platelets with development of pseudopods and centralization of granules closely surrounded by contractile microfilaments and supporting microtubules. The addition of palmitoyl-LPA and oleoyl-LPA, but not decanoyl-LPA, caused the release of calcium from a platelet membrane fraction that contains elements of the intracellular calcium storage system and actively concentrates this cation in the presence of adenosine triphosphate (ATP) and magnesium. It is suggested that LPAs cause aggregation by stimulating the release of calcium intracellularly.
Concentrations of concanavalin A or the calcium ionophore A23187 that are optimal for the transformation of pig or mouse lymphocytes do not normally cause a measurable increase in calcium influx compared with unstimulated cells. If the cells are treated with the mitogens in conditions where a measurable increase in calcium influx occurs, no stimulation of the cells can occur while the flux is maintained. If an early influx of extracellular calcium is necessary for stimulation, then a much smaller increase in the total concentration of cellular calcium than reported previously is sufficient to allow the entry of lymphocytes into the cell cycle.
Previous studies have demonstrated that phenytoin alters calcium conductance in isolated presynaptic nerve endings (synaptosomes) from rat or rabbit brain. Drug concentrations of 0.08 mM (20 microgram/ml) or higher inhibit stimulated calcium influx into synaptosomes depolarized by high concentrations of potassium (69 mM) by 7-58%. Calcium transport into undepolarized synaptosomes is only inhibited by 0.4 mM or greater concentrations of phenytoin. Recent investigations show that in mouse brain slices, phenytoin inhibited elevations of cyclic GMP and cyclic AMP produced by ouabain or veratridine. In contrast, elevations of the two cyclic nucleotides produced by high concentrations of potassium were not inhibited by phenytoin, suggesting that the anticonvulsant suppresses depolarization-induced elevation of cyclic nucleotide levels in brain slices by inhibiting influx of sodium into cells. These data indicate that phenytoin inhibits both sodium and calcium influx into cells during cellular depolarization and alters regulation of brain cyclic nucleotide levels. Both of these actions may be important for the antiepileptic effect of phenytoin.
Ionomycin, a recently discovered calcium ionophore, inhibits the ATP-dependent active Ca2+ transport of rabbit sarcoplasmic reticulum vesicles at concentrations as low as 10(-8) to 10(-6) M. The effect is due to an increase in the Ca2+ permeability of the membrane which is also observed on liposomes. The inhibition of Ca2+ uptake is accompanied by an increase in the Ca2+-sensitive ATPase activity of sarcoplasmic reticulum vesicles.
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The addition of 5-hydroxytryptamine to the isolated blowfly salivary gland stimulates fluid secretion, transepithelial calcium transport and the breakdown of 32P- or 3H-labelled phosphatidylinositol The breakdown of [32P]phosphatidylcholine and [32P]-phosphatidylethanolamine was not stimulated by 5-hydroxytryptamine. In salivary glands incubated with myo-[2-3H]inositol for 1--3 h, more than 95% of the label retained by the tissue was in the form of phosphatidylinositol. The addition of 5-hydroxytryptamine resulted in an increase in the accumulation of label in intracellular inositol 1:2-cyclic phosphate, inositol 1-phosphate and free inositol along with an increase in the release of [3H]inositol to the medium and saliva. The release of [3H]inositol to the medium served as a sensitive indicator of phosphatidylinositol breakdown. The release of [3H]inositol was not increased by cyclic AMP or the bivalent-cation ionophore A23187 under conditions in which salivary secretion was accelerated. The stimulation of fluid secretion by low concentrations of 5-hydroxytryptamine was potentiated by 3-isobutyl-1-methylxanthine, which had no effect on inositol release. The stimulation of fluid secretion by 5-hydroxytryptamine was greatly reduced in calcium-free buffer, but the breakdown of phosphatidylinositol continued at the same rate in the absence of calcium. These results support the hypothesis that breakdown of phosphatidylinositol by 5-hydroxytryptamine is involved in the gating of calcium.
We studied the effects of lidocaine (L) and chlorromazine (C), two compounds known to affect the binding of calcium to cell membranes, on histamine release and calcium uptake by purified mast cells upon challenge with the ionophore A23,187 or with compound 48/80. At low concentrations L and C inhibited the Ca++ flux as well as histamine release while higher concentration caused enhancement in this function. Evidence was obtained that L 10(-4) M may displace Ca++ from the cell membranes.
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