• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Chronic hypoxia selectively enhances L- and T-type voltage-dependent Ca~(2+) channel activity in pulmonary artery by upregulating Cav1.2 and Ca_v3.2.
【24h】

Chronic hypoxia selectively enhances L- and T-type voltage-dependent Ca~(2+) channel activity in pulmonary artery by upregulating Cav1.2 and Ca_v3.2.

机译：慢性缺氧通过上调Cav1.2和Ca_v3.2选择性增强肺动脉L型和T型电压依赖性Ca〜（2+）通道的活性。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hypoxia-induced pulmonary hypertension (HPH) is characterized by sustained pulmonary vasocon-striction and vascular remodeling, both of which are mediated by pulmonary artery smooth muscle cell (PASMC) contraction and proliferation, respectively. An increase in cytosolic Ca~(2+) concentration ([Ca~(2+)]_(cyt)) is a major trigger for pulmonary vasoconstriction and an important stimulus for cell proliferation in PASMCs. Ca~(2+) influx through voltage-dependent Ca~(2+) channels (VDCC) is an important pathway for the regulation of [Ca~(2+)]_(cyt). The potential role for L- and T-type VDCC in the development of HPH is still unclear. Using a hypoxic-induced pulmonary hypertension mouse model, we undertook this study to identify if VDCC in pulmonary artery (PA) are functionally upregulated and determine which type of VDCC are altered in HPH. Mice subjected to chronic hypoxia developed pulmonary hypertension within 4 wk, and high-K~+- and U-46619-induced contraction of PA was greater in chronic hypoxic mice than that in normoxic control mice. Additionally, we demonstrate that high-K~+-and U-46619-induced Ca~(2+) influx in PASMC is significantly increased in the hypoxic group. The VDCC activator, Bay K8864, induced greater contraction of the PA of hypoxic mice than in that of normoxic mice in isometric force measurements. L-type and T-type VDCC blockers significantly attenuated absolute contraction of the PA in hypoxic mice. Chronic hypoxia did not increase high-K~+- and U-46619-induced contraction of mesenteric artery (MA). Compared with MA, PA displayed higher expression of calcium channel voltage-dependent L-type alpha_(1c)-subunit (Ca_v1.2) and T-type alpha_(1H)-subunit (Ca_v3.2) upon exposure to chronic hypoxia. In conclusion, both L-type and T-type VDCC were functionally upregulated in PA, but not MA, in HPH mice, which could result from selectively increased expression of Ca_v1.2 and Ca_v3.2.
机译：缺氧性肺动脉高压（HPH）的特征在于持续的肺血管收缩和血管重塑，两者均分别由肺动脉平滑肌细胞（PASMC）的收缩和增殖介导。胞浆Ca〜（2+）浓度（[Ca〜（2 +）] _（cyt））的增加是肺血管收缩的主要诱因，也是PASMCs细胞增殖的重要刺激因素。 Ca〜（2+）通过电压依赖性Ca〜（2+）通道（VDCC）流入是调节[Ca〜（2 +）] _（cyt）的重要途径。 L型和T型VDCC在HPH发生中的潜在作用仍不清楚。使用低氧诱导的肺动脉高压小鼠模型，我们进行了这项研究，以确定肺动脉（PA）中的VDCC是否功能上调，并确定HPH中哪种类型的VDCC发生了改变。慢性缺氧小鼠在4 wk内出现肺动脉高压，慢性缺氧小鼠的高K〜+-和U-46619诱导的PA收缩大于正常氧对照小鼠。此外，我们证明低氧组中高钾离子和U-46619诱导的PASMC中Ca〜（2+）流入显着增加。在等距测力中，VDCC激活剂Bay K8864引起的缺氧小鼠的PA收缩比正常氧小鼠更大。在低氧小鼠中，L型和T型VDCC阻滞剂显着减弱了PA的绝对收缩。慢性缺氧并没有增加高钾离子和U-46619引起的肠系膜动脉（MA）的收缩。与MA相比，PA在暴露于慢性低氧时显示钙通道电压依赖性L型alpha_（1c）-亚基（Ca_v1.2）和T型alpha_（1H）-亚基（Ca_v3.2）更高的表达。总之，在HPH小鼠中，PA而非L型和T型VDCC在功能上均被上调，这可能是由于Ca_v1.2和Ca_v3.2的选择性表达增加所致。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号