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pubmed-article:11292181pubmed:dateCreated2001-4-6lld:pubmed
pubmed-article:11292181pubmed:abstractTextThe effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in HA22/VGH human hepatoma cells were evaluated using fura-2 as a fluorescent Ca2+ dye. Histamine (0.2-5 microM) increased [Ca2+]i in a concentration-dependent manner with an EC50 value of about 1 microM. The [Ca2+]i response comprised an initial rise, a slow decay, and a sustained phase. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In Ca2+-free medium, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 5 microM histamine failed to increase [Ca2+]i. After pretreatment with 5 microM histamine in Ca2+-free medium for 4 min, addition of 3 mM Ca2+ induced a [Ca2+]i increase of a magnitude 7-fold greater than control. Histamine (5 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 5 microM pyrilamine but was not altered by 50 microM cimetidine. Together, this study shows that histamine induced [Ca2+]i increases in human hepatoma cells by stimulating H1, but not H2, histamine receptors. The [Ca2+]i signal was caused by Ca2+ release from thapsigargin-sensitive endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, accompanied by Ca2+ entry.lld:pubmed
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pubmed-article:11292181pubmed:authorpubmed-author:LeeK CKClld:pubmed
pubmed-article:11292181pubmed:authorpubmed-author:WangJ LJLlld:pubmed
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pubmed-article:11292181pubmed:dateRevised2009-8-12lld:pubmed
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pubmed-article:11292181pubmed:articleTitleHistamine-Induced increases in intracellular free Ca2+ levels in hepatoma cells.lld:pubmed
pubmed-article:11292181pubmed:affiliationDepartment of Internal Medicine, Kaohsiung Veterans General Hospital, Taiwan, ROC.lld:pubmed
pubmed-article:11292181pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11292181pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed