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| 肾上腺髓质素对豚鼠心室肌细胞L-型钙通道的作用及其信号转导机制 | |
| 引用本文： | 柯琴梅,杜以梅,冯义柏,唐明,狄久芳.肾上腺髓质素对豚鼠心室肌细胞L-型钙通道的作用及其信号转导机制[J].中国病理生理杂志,2004,20(4):532-536. |
| 作者姓名： | 柯琴梅 杜以梅 冯义柏 唐明 狄久芳 |
| 作者单位： | 1. 华中科技大学同济医学院附属协和医院老年病科, 湖北 武汉 430022; 2. 华中科技大学同济医学院生理系, 湖北 武汉 430030; 3. 滕州中医院麻醉科, 山东 滕州 277500 |
| 基金项目： | 国家自然科学基金资助项目 (No .30 0 70 2 79) |
| 摘 要： | 目的: 研究肾上腺髓质素( adrenomedullin, ADM)抑制豚鼠心室肌细胞L-型钙通道的信号转导机制。方法: 应用全细胞膜片钳技术,记录应用ADM(1-100 nmol·L-1)前后L-型钙电流(ICa,L),以及分别记录应用ADM特异性受体拮抗剂ADM22-52(100 nmol·L-1)+ADM(100 nmol·L-1)、蛋白激酶A (PKA) 特异性拮抗剂H-89(10 μmol·L-1) + ADM(100 nmol·L-1)、蛋白激酶C (PKC) 特异性拮抗剂PKC19-36(10 μmol·L-1)+ADM(100 nmol·L-1)、PKC特异性激动剂PMA(1 μmol·L-1)前后ICa,L。结果: ADM(1-100 nmol·L-1)浓度依赖性地抑制豚鼠心室肌细胞ICa,L,并可被ADM22-52(100 nmol·L-1)完全阻断;H-89(10 μmol·L-1)对ADM抑制ICa,L的作用无影响。PKC19-36(10 μmol·L-1)可完全阻断ADM 对ICa,L的抑制效应,且PMA(1 μmol·L-1)可模拟ADM 对ICa,L的抑制效应。结论: ADM作用于特异性ADM受体可浓度依赖性地抑制豚鼠心室肌细胞ICa,L,此作用有可能与PKC激活相关。 |
| 关 键 词： | 肾上腺髓质素 钙通道 L-型 心肌 信号转导 |
| 文章编号： | 1000-4718(2004)04-0532-05 |
| 收稿时间： | 2003-08-13 |
Effect of adrenomedullin on L-type calcium currents and its signaling transduction process in guinea-pig ventricular myocytes |
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| KE Qin-mei,DU Yi-mei,FENG Yi-bai,TANG Ming,DI Jiu-fang.Effect of adrenomedullin on L-type calcium currents and its signaling transduction process in guinea-pig ventricular myocytes[J].Chinese Journal of Pathophysiology,2004,20(4):532-536. | |
| Authors: | KE Qin-mei DU Yi-mei FENG Yi-bai TANG Ming DI Jiu-fang |
| Affiliation: | 1. Department of Geriatrics, The Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; 2. Department of Physiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; 3. Department of Anesthesiology, Tengzhou Hospital of Traditional Chinese Medicine, Tengzhou 277500, China |
| Abstract: | AIM: To study the effect of adrenomedullin (ADM) on L-type calcium currents (ICa,L) and its signaling transduction process in guinea-pig ventricular myocytes. METHODS: By using whole-cell patch clamp technique, the effect of ADM(1-100 nmol·L-1) on ICa,L was investigated in enzymatically dispersed single guinea-pig ventricular myocyte. Furthermore, the possible signaling transduction process of ADM on ICa,L was investigated by observing the effects of ADM22-52 (a specific ADM-receptor antagonist,100 nmol·L-1)+ADM(100 nmol·L-1), H-89 (a specific protein kinase A inhibitor, 10 μmol·L-1) + ADM(100 nmol·L-1), PKC19-36 (a specific protein kinase C inhibitor, 10 μmol·L-1) + ADM(100 nmol·L-1) and PMA (a specific protein kinase C activator, 1 μmol·L-1) on ICa,L, respectively. RESULTS: ADM at the concentrations of 1-100 nmol·L-1 decreased ICa,L in a dose-dependent manner (P<0.05) and ADM22-52 completely abolished the ADM-induced inhibition of ICa,L. H-89 did not attenuate the effects of ADM on ICa,L. Intracellular application of PKC19-36 prevented ADM-induced inhibition of ICa,L, while PMA could mimic the effects of ADM on ICa,L. CONCLUSION: ADM inhibits ICa,L, in guinea-pig ventricular myocytes, which is mediated by the specific ADM-receptor and probably related to PKC pathway. |
| Keywords: | Adrenomedullin Calcium channels L-type Myocardium Signal transduction |
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