Effects of loratadine on cytosolic Ca2+ levels and leukotriene release: novel mechanisms of action independent of the anti-histamine activity.

doi:10.1016/0922-4106(94)90130-9

Paper

Effects of loratadine on cytosolic Ca2+ levels and leukotriene release: novel mechanisms of action independent of the anti-histamine activity.

Published Feb 15, 1994 · O. Letari, Amelia Miozzo, G. Folco

European journal of pharmacology

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38

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Abstract

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In Vitro Study

Study Snapshot

Loratadine may have anti-allergic properties by interfering with calcium release mechanisms, inhibiting cell activation, and potentially aiding in the study of calcium homeostasis.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Effects of loratadine on cytosolic Ca2+ levels and leukotriene release: novel mechanisms of action independent of the anti-histamine activity.

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References

Activation by bacterial lipopolysaccharide causes changes in the cytosolic free calcium concentration in single peritoneal macrophages.

LPS-induced increases in macrophage cytosolic free calcium concentration support the hypothesis that calcium is a second messenger in LPS-mediated macrophage activation.

Direct airway injury results in elevated levels of sulfidopeptide leukotrienes, detectable in airway secretions.

Elevated airway leukotriene levels in tracheal secretions may reflect airway epithelial damage but may not predict the development of Adult Respiratory Distress Syndrome (ARDS).

Cytosolic calcium ion and arachidonic acid release and metabolism in macrophages.

Cytosolic calcium ion increase is not necessary for arachidonic acid release and metabolism in rat peritoneal macrophages.

Inhibitory effect of terfenadine on mediator release from human blood basophils and eosinophils

Terfenadine, in addition to its known antihistaminic properties, also has an inhibitory effect on chemical mediator release from human blood basophils and eosinophils.

Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulates calcium fluxes at the plasma membrane.

Phasigargin activates calcium entry in parotid acinar cells by depleting the intracellular inositol 1,4,5-trisphosphate-sensitive Ca2+ pool, and calcium entry occurs directly across the plasma membrane to the cytoplasm rather than through a cycle of uptake

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