Ikeda H, Kubo N, Nakamura A, Harada N, Minamino M, Yamashita T
Department of Otolaryngology, Kansai Medical University, Osaka, Japan.
Acta Otolaryngol. 1997 Nov;117(6):864-70. doi: 10.3109/00016489709114216.
Changes in cytosolic Ca2+ concentration ([Ca2+]i) in cultured human mucosal microvascular endothelial cells (HMMECs) from nasal inferior turbinate were measured using a fluorescent Ca(2+)-sensitive dye, fura-2, and photometric fluorescence microscopy. Histamine caused a transient increase in intracellular free Ca2+ in cell populations and in individual cells, followed by a decrease to a sustained elevation. Histamine (100 microM) elevated [Ca2+]i in HMMECs up to 563 +/- 20 nM from a resting level of 60 +/- 45 nM (means +/- SD, n = 31). Promethazine (a histamine H1 receptor antagonist) inhibited [Ca2+]i increase during histamine stimulation, whereas cimetidine (a H2 receptor antagonist) and thioperamide (a H3 receptor antagonist) showed no inhibition. These results suggest that the histamine increase [Ca2+]i in HMMECs induces both a Ca2+ release from stores and a Ca2+ influx through activation of the H1 receptor.
采用荧光钙敏染料fura-2和光度荧光显微镜，测量了来自下鼻甲的培养人鼻粘膜微血管内皮细胞（HMMECs）胞质Ca2+浓度（[Ca2+]i）的变化。组胺引起细胞群体和单个细胞内游离Ca2+的瞬时增加，随后下降至持续升高。组胺（100μM）使HMMECs中的[Ca2+]i从静息水平60±45 nM升高至563±20 nM（平均值±标准差，n = 31）。异丙嗪（一种组胺H1受体拮抗剂）在组胺刺激期间抑制[Ca2+]i增加，而西咪替丁（一种H2受体拮抗剂）和硫代酰胺（一种H3受体拮抗剂）则无抑制作用。这些结果表明，组胺使HMMECs中的[Ca2+]i增加，通过激活H1受体诱导Ca2+从储存库释放和Ca2+内流。
