Mislocalization of eNOS and upregulation of cerebral vascular Ca2+ channel activity in angiotensin-hypertension
Mislocalization of eNOS and upregulation of cerebral vascular Ca2+ channel activity in angiotensin-hypertension
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DOI：
10.1161/01.hyp.0000066288.20169.21
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发表时间：
2003-05-01
期刊：
影响因子：
8.3
通讯作者：
Simard, JM
中科院分区：
文献类型：
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作者：
Gerzanich, V;Ivanova, S;Simard, JM
我们验证了血管紧张素II （Ang-hypertension）诱导的内皮功能障碍会损害内皮型一氧化氮合酶（eNOS）对血管平滑肌l型Ca2+通道的调节控制的假设。我们研究了正常血压大鼠(240 μ g.kg（-1).h(-1) SQ × 4天）和高血压大鼠(AHR; 240 μ g.kg（-1).h（-1） × 28天）的脑皮层纹状体小动脉（LSAs）。膜片钳对分离的LSA平滑肌细胞（SMCs）的测量显示，与对照组相比，4天和28天输注的Ca2+通道可用性显著增加（分别为0.47+/-0.03和0.66+/-0.05 vs 0.36+/-0.03 pS/pF）
We tested the hypothesis that endothelial dysfunction induced by angiotensin II (Ang-hypertension) would impair regulatory control of vascular smooth muscle L-type Ca2+ channels by endothelial nitric oxide synthase (eNOS). We studied cerebral lenticulostriate arterioles (LSAs) from control rats, from rats infused with Ang (240 mug.kg(-1).h(-1) SQ x4 days), which were normotensive, and from Ang-hypertensive rats (AHR; 240 mug.kg(-1).h(-1) x28 days). Patch-clamp measurements on isolated LSA smooth muscle cells (SMCs) showed a significant increase in Ca2+ channel availability with 4- and 28-day infusions versus controls (0.47+/-0.03 and 0.66+/-0.05 vs 0.36+/-0.03 pS/pF, respectively; P