Involvement of prostaglandins in histamine H-1 receptor-operated Ca2+ entry in human gingival fibroblasts

In the absence of external Ca2+, 100 mu M histamine evoked a transient incr ease in intracellular Ca2+ ([Ca2+](i)), and subsequent addition of Ca2+ to the medium resulted in a sustained increase in [Ca2+](i) in fura-2-loaded h uman gingival fibroblasts. These Ca2+ mobilizations are attributed to Ca2release from intracellular stores and Ca2+ entry, respectively. When the hi stamine H-1 antagonist chlorpheniramine was added after the histamine-induc ed transient increase in [Ca2+](i), the Ca2+ entry induced by the addition of Ca2+ was inhibited. In the fibroblasts pretreated with cyclooxygenase in hibitors, indomethacin (1 mu M) or aspirin (100 mu M), histamine-induced Ca 2+ entry was significantly inhibited, but not the transient [Ca2+](i) incre ase. These results suggest that the histamine-induced Ca2+ entry requires t he continuous binding of histamine to the H-1 receptors and is regulated by prostaglandins, which are probably produced due to the H-1 receptor activa tion. (C) 1998 Elsevier Science Inc.