Ricciardolo F L, Lovett M, Halliday D A, Nadel J A, Kaneko T, Bunnett N W, Geppetti P
Institute of Respiratory Disease, University of Catania, Italy.
Inflamm Res. 1998 May;47(5):231-5. doi: 10.1007/s000110050322.
To determine which types of kinin receptor are present in human bronchial epithelial cells we studied the capability of bradykinin to mobilize intracellular Ca2+ ([Ca2+]i) in a human bronchial epithelial cell line (16HBE cells).
Human bronchial epithelial cell line transformed with an original defective simian virus 40 (SV40).
Bradykinin (0.1 pM to 0.1 microM), des-Arg9 bradykinin (1 microM), des-Arg10) kallidin (1 microM), indomethacin (1 microM), phosphoramidon (1 microM), captopril (1 microM), des-Arg9-[Leu8]bradykinin (1 microM), HOE 140 (DArg-[Hyp3, Thi5, DTic , Oic8]-bradykinin) (1 microM), and NPC 16731 (DArg-[Hyp3, Thi5, DTic7, Tic8]-bradykinin) (1 microM).
The mobilization of [Ca2+]i was determined by the fura-2 method. Two sample Wilcoxon rank-sum (Mann-Whitney) test was used for statistical calculations.
Bradykinin, but not the selective agonists for kinin B1 receptor des-Arg9 bradykinin and des-Arg10 kallidin, increased the mobilization of [Ca2+]i (EC50, 0.079+/-0.009nM) in 16HBE cells in a concentration-dependent manner. Pretreatment with the cyclooxygenase inhibitor indomethacin (1 microM) or the peptidase inhibitors, phosphoramidon (1 microM) or captopril (1 microM), did not affect the response to bradykinin. The kinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin (1 microM), was inactive. HOE 140 and NPC 16731, two selective antagonists of the kinin B2 receptor abolished the response to bradykinin (IC50 of HOE 140 and NPC 16731 were 0.52+/-0.037nM and 1.67 +/- 0.41 nM, respectively).
The present data indicate the presence of kinin B2 receptors in the 16HBE cells.
为了确定人类支气管上皮细胞中存在哪些类型的激肽受体，我们研究了缓激肽在一种人类支气管上皮细胞系（16HBE细胞）中动员细胞内钙离子（[Ca2+]i）的能力。
用原始缺陷型猿猴病毒40（SV40）转化的人类支气管上皮细胞系。
缓激肽（0.1 pM至0.1 microM）、去-精氨酸9缓激肽（1 microM）、去-精氨酸10胰激肽（1 microM）、吲哚美辛（1 microM）、磷酰胺（1 microM）、卡托普利（1 microM）、去-精氨酸9-[亮氨酸8]缓激肽（1 microM）、HOE 140（D-精氨酸-[Hyp3, Thi5, DTic, Oic8]-缓激肽）（1 microM）和NPC 16731（D-精氨酸-[Hyp3, Thi5, DTic7, Tic8]-缓激肽）（1 microM）。
采用fura-2法测定[Ca2+]i的动员情况。统计计算采用两样本Wilcoxon秩和（Mann-Whitney）检验。
缓激肽能以浓度依赖性方式增加16HBE细胞中[Ca2+]i的动员（EC50，0.079±0.009 nM），而去-精氨酸9缓激肽和去-精氨酸10胰激肽这两种激肽B1受体的选择性激动剂则不能。用环氧化酶抑制剂吲哚美辛（1 microM）或肽酶抑制剂磷酰胺（1 microM）或卡托普利（1 microM）预处理，不影响对缓激肽的反应。激肽B1受体拮抗剂去-精氨酸9-[亮氨酸8]缓激肽（1 microM）无活性。HOE 140和NPC 16731这两种激肽B2受体的选择性拮抗剂可消除对缓激肽的反应（HOE 140和NPC 16731的IC50分别为0.52±0.037 nM和1.67±0.41 nM）。
目前的数据表明16HBE细胞中存在激肽B2受体。
