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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-8-15
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0953-7104
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-65
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Intracellular alkalinization augments platelet aggregation due to increase in cytosolic free-Ca2+.
pubmed:affiliation
Department of Hygiene and Preventive Medicine, School of Medicine, Yamagata University, Japan.
pubmed:publicationType
Journal Article