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首页> 外文期刊>Pfluegers Archiv: European Journal of Physiology >Deletion of T-type calcium channels Ca(v)3.1 or Ca(v)3.2 attenuates endothelial dysfunction in aging mice
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Deletion of T-type calcium channels Ca(v)3.1 or Ca(v)3.2 attenuates endothelial dysfunction in aging mice

机译：缺失T型钙通道Ca（v）3.1或Ca（v）3.2衰减老化小鼠的内皮功能障碍

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Impairment of endothelial function with aging is accompanied by reduced nitric oxide (NO) production. T-type Ca(v)3.1 channels augment nitric oxide and co-localize with eNOS. Therefore, the hypothesis was that T-type channels contribute to the endothelial dysfunction of aging. Endothelial function was determined in mesenteric arteries (perfusion) and aortae (isometric contraction) of young and old wild-type (WT), Ca(v)3.1, and Ca(v)3.2 knockout mice. NO production was measured by fluorescence imaging in mesenteric arteries. With age, endothelium-dependent subsequent dilatation (following depolarization with KCl) of mesenteric arteries was diminished in the arteries of WT mice, unchanged in Ca(v)3.2(-/-) preparations but increased in those of Ca(v)3.1(-/-) mice. NO synthase inhibition abolished the subsequent dilatation in mesenteric arteries and acetylcholine-induced relaxations in aortae. NO levels were significantly reduced in mesenteric arteries of old compared to young WT mice. In Ca(v)3.1(-/-) and Ca(v)3.2(-/-) preparations, NO levels increased significantly with age. Relaxations to acetylcholine were significantly smaller in the aortae of old compared to young WT mice, while such responses were comparable in preparations of young and old Ca(v)3.1(-/-) and Ca(v)3.2(-/-) mice. The expression of Ca(v)3.1 was significantly reduced in aortae from aged compared to young WT mice. The level of phosphorylated eNOS was significantly increased in aortae from aged Ca(v)3.1(-/-) mice. In conclusion, T-type calcium channel-deficient mice develop less age-dependent endothelial dysfunction. Changes in NO levels are involved in this phenomenon in WT and Ca(v)3.1(-/-) mice. These findings suggest that T-type channels play an important role in age-induced endothelial dysfunction.
机译：衰老内皮功能的损伤伴随着减少的一氧化氮（NO）生产。 T型CA（V）3.1通道增强一氧化氮，并与eNOS共定位。因此，假设是T型通道有助于老化的内皮功能障碍。内皮函数在患有幼年和旧野生型（WT），Ca（v）3.1和Ca（v）3.2敲除小鼠中的肠系膜术动脉（灌注）和主动脉（均衡）和Aortae（等距收缩）中测定。在肠系膜中的荧光成像中没有产生生产。随着年龄的增长，在WT小鼠的动脉中，在Ca（v）3.2（ - / - ）制剂中不变，肠系膜动脉依赖于肠系膜动脉的肠系膜动脉依赖性肠道膨胀（在KCl脱落后）减少，但在Ca（v）3.1（ -/-） 老鼠。没有废除合酶在肠系膜动脉和乙酰胆碱诱导的主动脉中的膨胀中的膨胀。与年轻的WT小鼠相比，肠系膜动脉中没有显着降低水平。在Ca（v）3.1（ - / - ）和Ca（v）3.2（ - / - ）制剂，年龄没有显着增加。与杨氏小鼠相比，古代的Aortae在乙酰胆碱的放松显着较小，而这些反应在杨和旧的Ca（v）3.1（ - / - ）和Ca（ - / - ）小鼠的制备中是可比的。与年轻的WT小鼠相比，Aortae的Ca（v）3.1的表达显着降低。来自Aged Ca（v）3.1（ - / - ）小鼠的Aortae中，磷酸化烯的水平显着增加。总之，T型钙通道缺陷小鼠产生较少的年龄依赖性内皮功能障碍。在WT和Ca（v）3.1（ - / - ）小鼠中，没有水平的变化涉及这种现象。这些发现表明T型通道在年龄诱导的内皮功能障碍中起着重要作用。

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