We characterized the effects of histamine on intracellular Ca2+ and activation of ionic currents in human capillary endothelial cells. Histamine produced both a transient and sustained increase in intracellular Ca2+. The transient response was mediated largely through intracellular Ca2+ release and the sustained response was due to extracellular Ca2+ entry. The increase in intracellular Ca2+ by histamine was not affected by the H2 blocker cimetidine. But was entirely blocked by the H1 antagonist diphenhydramine showing that the histamine response in these cells is mediated through the H1 receptor. A transient ionic current is coactivated with the histamine-induced increase in intracellular Ca2+ and this current has several properties of a nonselective, Ca2+ permeable, cation channel (NSC). The magnitude of the NSC current does not strictly correlate with intracellular Ca2+ levels. A Ca2+-activated K+ current (BKCA) is activated by the increase in intracellular Ca2+ and this current is blocked by the selective BKCA blocker iberiotoxin.
The Journal of Membrane Biology – Springer Journals
Published: Jan 15, 2000
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