Deficiency of Nox2 prevents angiotensin II-induced inward remodeling in cerebral arterioles.
Deficiency of Nox2 prevents angiotensin II-induced inward remodeling in cerebral arterioles.
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DOI：
10.3389/fphys.2013.00133
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发表时间：
2013
影响因子：
4
通讯作者：
Baumbach GL
中科院分区：
文献类型：
--
作者：
Chan SL;Baumbach GL
血管紧张素II是脑小动脉向内重塑的重要决定因素。血管紧张素 II 的许多血管作用是由 NADPH 氧化酶同系物产生的活性氧 (ROS) 介导的，其中 Nox2 在小动脉和小动脉中占主导地位。因此，我们检验了 Nox2 产生的超氧化物在血管紧张素 II 诱导的脑小动脉重塑中发挥作用的假设。我们检查了 Nox2 缺陷型和野生型 (WT) 小鼠，其中通过渗透微型泵输注升压或非升压剂量的血管紧张素 II（1000 或 200 ng/kg/天）或盐水 4 周。收缩动脉压通过尾套法测量。通过麻醉小鼠的开放颅窗测量脑动脉的压力和直径。离体测定脑小动脉的横截面积（通过组织学）和超氧化物水平（通过氢化乙啶染色）。血管紧张素 II 的升压剂量（而非非升压剂量）显着增加了 WT 和 Nox2 缺陷小鼠的收缩动脉压。两种剂量的血管紧张素 II 均可增加 WT 小鼠最大扩张脑小动脉的超氧化物水平并显着减小外径。 Nox2缺陷小鼠中超氧化物的增加和向内重塑被阻止。此外，只有 AngII 的加压剂量才能增加 WT 小鼠的小动脉壁横截面积，而在 Nox2 缺陷小鼠中则受到阻止。总之，源自含Nox2的NADPH氧化酶的超氧化物在血管紧张素II介导的脑小动脉向内重塑中发挥重要作用。这种效应似乎与压力无关，并且与肥大的效应不同。
Angiotensin II is an important determinant of inward remodeling in cerebral arterioles. Many of the vascular effects of angiotensin II are mediated by reactive oxygen species (ROS) generated from homologs of NADPH oxidase with Nox2 predominating in small arteries and arterioles. Therefore, we tested the hypothesis that superoxide generated by Nox2 plays a role in angiotensin II-induced cerebral arteriolar remodeling. We examined Nox2-deficient and wild-type (WT) mice in which a pressor or a non-pressor dose of angiotensin II (1000 or 200 ng/kg/day) or saline was infused for 4 weeks via osmotic minipumps. Systolic arterial pressure was measured by a tail-cuff method. Pressure and diameter of cerebral arterioles were measured through an open cranial window in anesthetized mice. Cross-sectional area (by histology) and superoxide level (by hydroethidine staining) of cerebral arterioles were determined ex vivo. The pressor, but not the non-pressor, dose of angiotensin II significantly increased systolic arterial pressure in both WT and Nox2-deficient mice. Both doses of angiotensin II increased superoxide levels and significantly reduced external diameter in maximally dilated cerebral arterioles in WT mice. Increased superoxide and inward remodeling were prevented in Nox2-deficient mice. Moreover, only the pressor dose of AngII increased cross-sectional area of arteriolar wall in WT mice and was prevented in Nox2-deficient mice. In conclusion, superoxide derived from Nox2-containing NADPH oxidase plays an important role in angiotensin II-mediated inward remodeling in cerebral arterioles. This effect appears to be independent of pressure and different from that of hypertrophy.
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影响因子：
20.1
作者：
BAUMBACH, GL;DOBRIN, PB;HEISTAD, DD
通讯作者：
HEISTAD, DD
DOI：
10.1152/ajpheart.00079.2002
发表时间：
2002-10-01
影响因子：
4.8
作者：
Didion, SP;Ryan, MJ;Faraci, FM
通讯作者：
Faraci, FM
影响因子：
15.9
作者：
DUBEY, RK;JACKSON, EK;LUSCHER, TF
通讯作者：
LUSCHER, TF
影响因子：
20.1
作者：
GRIENDLING, KK;MINIERI, CA;ALEXANDER, RW
通讯作者：
ALEXANDER, RW
DOI：
10.1152/ajpheart.01066.2010
发表时间：
2011-06-01
影响因子：
4.8
作者：
Martinez-Lemus, Luis A.;Zhao, Guiling;Boone, Matthew
通讯作者：
Boone, Matthew