Elife:科学家有望开发出治疗高血压的新型靶向性药物疗法

2018-12-11 佚名 细胞

近日,一项刊登在国际杂志eLife上的研究报告中,来自美国田纳西大学健康科学研究中心的科学家们通过研究在血压调节过程中鉴别出了一种关键分子,通过关闭该分子的功能就能够有效降低小鼠机体的血压。

近日,一项刊登在国际杂志eLife上的研究报告中,来自美国田纳西大学健康科学研究中心的科学家们通过研究在血压调节过程中鉴别出了一种关键分子,通过关闭该分子的功能就能够有效降低小鼠机体的血压。

这项研究结束了科学家们关于这种分子对高血压影响的不确定性,有望帮助开发新型高血压药物;如今高血压在全球影响着数百万人的健康,其也是引发心脏病发作和中风的主要风险因素。血压受到了机体血管壁肌肉细胞的部分控制,这些肌肉细胞表面携带有名为瞬时受体电位通道(TRP通道)的特殊蛋白,其能促进钠和钙移动;动脉肌肉细胞中存在有大约13种不同的TRP通道,目前研究人员并不清楚是否这些通道控制着机体正常的血压或帮助促进高血压的发生。

研究者Jonathan Jaggar教授说道,目前研究人员并不清楚是否TRP通道会促进正常血压还是改变正常血压,同时他们也不知道不同器官中不同类型的通道是否会以相似的方式被控制;随后研究人员选择了一种名为PKD2的TRP通道进行研究,因为该蛋白发生遗传突变的患者常常患有高血压,而且此前研究结果在动脉肌肉细胞的相关功能上得出了相互矛盾的结果。

文章中,研究者关闭了小鼠平滑肌细胞中的PKD2,随后发现,相比正常小鼠而言,这些小鼠机体的血压发生下降了,随后研究者通过增加小鼠下肢血管中的压力来观察小鼠机体血管的收缩情况,他们发现,血压的升高增加了功能性PKD2小鼠机体的血管收缩,但对于不携带PKD2的小鼠却没有影响,PKD2并不会诱发两种血管收缩分子的效应(去氧肾上腺素和血管紧张素II)。

相比之下,当研究人员观察小鼠下腹部的动脉时他们发现,PKD2会促进去氧肾上腺素所诱发的血管收缩,这就表明,特殊的血管收缩刺激剂会激活机体不同组织动脉中的PKD2通道;PKD2的激活能够促进钠离子进入细胞,从而改变肌肉细胞的膜电位,并诱发血管发生收缩。下一步研究人员将会检测一种假设,即移除PKD2是否会降低小鼠机体中的高血压,随后研究者给予正常和PKD2缺陷小鼠注入血管紧张素II(其能帮助升高血压),结果发现,正常小鼠机体中动脉血压的增加比PKD2缺失小鼠低26%,而且高血压小鼠机体的动脉肌肉细胞表面的PKD2水平较高。

当利用去氧肾上腺素治疗后,研究人员测定了处于高血压状态下机体血管的收缩特性,结果表明,PKD2缺失的小鼠机体血管收缩仅为正常小鼠大约70%,这就证实,PKD2缺失的小鼠机体中血压的降低或许源于血管的松弛,最后研究者Jaggar总结道,本文研究结果表明,能够激活PKD2通道的刺激剂或许具有血管特异性,这就表明,在所有动脉中并没有一种单一的机制能够调节肌肉细胞的收缩性。

阐明肌肉细胞PKD2通道能够调节血压或许能够帮助研究人员更好地理解离子通道靶点在正常心血管生理学中的重要性,同时其或许还能作为一种潜在的药物靶点帮助开发治疗心血管疾病的新型疗法。

原始出处:

Simon Bulley,et al. Arterial smooth muscle cell PKD2 (TRPP1) channels regulate systemic blood pressure.Elife. 2018 Dec 4;7. pii: e42628.

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    2019-10-15 膀胱癌
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    2019-02-03 clmlylxy
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    2018-12-12 kafei

    学习了谢谢

    0

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    2018-12-11 医者仁心5538

    学习了。继续努力,希望早日用于临床。

    0

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