cysteinyl-leukotriene D4诱导胞质Ca2 +高程和人类逼尿肌的收缩肌肉。

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安德森Bouchelouche K, L, Nordling J,角T, Bouchelouche P

cysteinyl-leukotriene D4诱导胞质Ca2 +高程和人类逼尿肌的收缩肌肉。

8月杂志。2003;170 (2 Pt 1): 638 - 44。

PubMed ID

12853847 (在PubMed

]

文摘

目的:细胞内钙离子的作用在人类逼尿肌的激活平滑肌细胞(smc)是关键。最近我们发现肥大细胞衍生促炎介质白三烯D(4)((4))诱发细胞内自由钙离子增加([Ca2 +] (i))在人类逼尿肌细胞。有限公司在当前的研究中,我们调查了机制(4)诱导增加[Ca2 +] (i)和测试有限公司(4)是否诱发肌肉收缩力通过测量人类逼尿肌组织的发展。材料与方法:文化的人类逼尿肌smc得到良性膀胱疾病患者进行膀胱镜检查。[Ca2 +](我)测量fura-2 smc用micro-spectrofluorometry加载和动态视频成像。收缩力监测特别是mini-myograph建造。结果:自发振荡(Ca2 +) (i)和观察。在缺乏钙这些振荡缺席。有限公司(4)引起的浓度依赖性增加[Ca2 +] (i)和等距力量。钙释放全部来自细胞内的商店。 Increases in [Ca2+](i) and force were inhibited in dose dependent fashion by the LTD(4) receptor antagonists montelukast and zafirlukast. Likewise, LTC(4) and LTE(4) induced an increase in [Ca2+](i) and contractile force in the rank order LTD(4) >LTC(4) >LTE(4). Inhibition of Ca2+ induced Ca2+ release (CICR) with thapsigargin and ryanodine suggested the presence of a functional CICR in SMCs. CONCLUSIONS: To our knowledge this study demonstrates for the first time that the cysteinyl-leukotriene LTD(4) induces contraction in human detrusor SMCs. LTD(4) induced force and increased [Ca2+](i) were entirely dependent on Ca2+ release from intracellular stores. The action of LTD(4) on force development and increased [Ca2+](i) appeared to be specific, mediated by the binding and activation of specific LTD(4) receptors on SMCs. Also, to our knowledge this report is the first to show that human detrusor SMCs are sensitive to ryanodine, consistent with the hypothesis that a CICR is present and functional in these cells. The presence and role of endogenous cysteinyl leukotrienes for normal contractile functioning of the human detrusor during inflammation remains to be elucidated.

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药物靶点

药物	目标	类	生物	药理作用	行动
白三烯C4	半胱氨酰白三烯受体1	蛋白质	人类	未知的	不可用	细节
白三烯D4	半胱氨酰白三烯受体1	蛋白质	人类	未知的	不可用	细节