HCO3(-) ions increase mast cell sensitivity to thapsigargin-induced Ca(2+) entry

Area of Science:

• * Immunology
• * Cell Physiology

Background:

• * Calcium (Ca2+) entry into rat mast cells is influenced by external ions.
• * Bicarbonate (HCO3-) ions are known to modulate mast cell degranulation.
• * The interaction between HCO3- and Ca2+ entry, particularly in response to thapsigargin, requires further investigation.

Purpose of the Study:

• * To investigate the regulatory role of HCO3- ions on Ca2+ entry in rat mast cells.
• * To explore the relationship between HCO3(-)-modulated Ca2+ entry and exocytosis.
• * To determine how HCO3- influences mast cell degranulation.

Main Methods:

• * Measurement of Ca2+ entry in rat mast cells using a thapsigargin-activated model.
• * Comparison of Ca2+ entry and exocytosis in HCO3(-)-buffered versus HCO3(-)-free media.
• * Assessment of intracellular Ca2+ ([Ca2+]i) levels and degranulation in response to varying HCO3- concentrations.

Main Results:

• * Both Ca2+ entry and exocytosis were enhanced in the presence of HCO3- ions.
• * Mast cells with elevated intracellular Ca2+ ([Ca2+]i) underwent degranulation in a HCO3(-)-buffered medium.
• * While a HCO3(-)-free medium showed a higher second Ca2+ entry, degranulation remained low, indicating HCO3-'s essential role.

Conclusions:

• * HCO3- ions significantly increase capacitative Ca2+ entry in rat mast cells.
• * HCO3- enhances the sensitivity of mast cells to intracellular Ca2+, promoting degranulation.
• * Bicarbonate is a key regulator of both Ca2+ influx and exocytosis in mast cells.