Intracellular alkalinization augments platelet aggregation due to increase in cytosolic free-Ca2+
| Autor: | Ichiro Wakabayashi, Mikio Marumo, Eizo Kakishita, Akira Suehiro |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Platelet aggregation
Platelet Aggregation Intracellular pH Ionomycin Stimulation Hematology General Medicine Hydrogen-Ion Concentration Ammonium Chloride chemistry.chemical_compound Cytosol Kinetics Biochemistry chemistry Nephelometry and Turbidimetry Biophysics Humans Platelet Calcium Platelet activation Intracellular alkalinization |
| Zdroj: | Platelets. 13(3) |
| ISSN: | 0953-7104 |
| Popis: | Intracellular pH is known to increase during agonist-induced platelet activation. In order to elucidate the role of intracellular alkalinization in platelet activation, the effects of NH4Cl, as a tool to induce intracellular alkalinization, on ionomycin-induced platelet activation were investigated. NH4Cl (2.5-10 mM) concentration-dependently induced intracellular alkalinization. Platelet aggregation induced by ionomycin (0.1 microM) was augmented by treatment with NH4Cl (2.5-10 mM). Ionomycin-induced platelet aggregation in the absence of extraplatelet Ca2+, which was markedly attenuated compared to that in the presence of extraplatelet Ca2+, was also augmented by NH4Cl. NH4Cl treatment increased the number of large aggregates after ionomycin stimulation, while it decreased the number of small aggregates. Both transplasmalemmal Ca2+ entry and intracellular Ca2+ release induced by ionomycin were increased by treatment with NH4Cl (10 mM). SKF-96365 (100 microM), an inhibitor of receptor-operated Ca2+ channels, did not affect ionomycin-induced Ca2+ entry but abolished the effect of NH4Cl on Ca2+ entry. Thus, NH4Cl augments receptor-operated Ca2+ channels and intracellular Ca2+ release. These findings suggest that intracellular alkalinization plays a significant role in agonist-induced platelet activation. |
| Databáze: | OpenAIRE |
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