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作 者:杨朝[1] 张珍祥[1] 徐永健[1] 汪涛[1] 倪望[1] 李亚清[1]
机构地区:[1]华中科技大学同济医学院附属同济医院卫生部呼吸系疾病重点实验室,武汉430030
出 处:《华中科技大学学报(医学版)》2007年第1期27-30,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
摘 要:目的观察大鼠肺动脉平滑肌细胞(PASMCs)膜钙激活氯通道(ClCa)与细胞质钙的关系及意义。方法大鼠PASMCs获取采用急性酶分离法。荧光光度法检测细胞质内游离钙离子浓度([Ca2+]i);全细胞膜片钳技术测定PASMCs钙激活氯电流(ICl(Ca));等长张力测定法观察ClCa阻滞剂尼氟灭酸(NFA)和Indaryloxyacetic acid(IAA-94)对大鼠肺动脉张力的影响。结果环匹阿尼酸(CPA)和苯福林(PE)均可引起[Ca2+]i升高;升高的[Ca2+]i可以引出ICl(Ca);NFA和IAA-94可以舒张CPA、PE引起的肺动脉环收缩。结论生理条件下大鼠PASMCs的ClCa是钙依赖性的;细胞外Ca2+内流及细胞质内Ca2+释放均可激活该通道,其参与了血管活性药诱导的肺动脉收缩。Objective To investigate the relationship between calcium-activated chloride (ClCa) channels and calcium of cytoplasm of pulmonary artery smooth muscle cells (PASMCs) in rats. Methods PASMCs were obtained by the acute enzyme separation method. Cytoplasmic free Ca^2+ concentration ([Ca^2+]i) in PASMCs was investigated by fluorophotometry. Ca^2+-activated Cl^- currents (ICl(Ca)) were recorded by the conventional whole-cell patch clamp technique. The regulating effects of the ClCa channel blockers niflumic acid (NFA) and indaryloxyacetic acid (IAA-94) on the tone of pulmonary artery smooth muscle were observed by measuring the isometric tone of pulmonary artery rings in vitro. Results Cyclopiazonic acid (CPA) and phenylephrine (PE) could increase [Ca^2+]i. The NFA and IAA-94 significantly and reversibly inhibited the ICl(Ca) induced by increased [Ca^2+]i. The NFA and IAA-94 produced inhibitory effects on CPA-induced or PE-induced contractions in the pulmonary artery. Conclusion ClCa channels are depended on [Ca^2+]i in PASMCs. An increase in [Ca^2+]i, via Ca^2+ influx or release, activates ClCa channels and induces ICl(Ca). This Cl^- current contributes to the agonist-induced tension under physiological conditions.
关 键 词:钙激活氯通道 膜片钳 肺动脉平滑肌细胞 钙离子 血管张力
分 类 号:R338[医药卫生—人体生理学] R965[医药卫生—基础医学]
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