Functional integrity of endothelium determines Ca2+ channel availability in smooth muscle:: involvement of nitric oxide
Functional integrity of endothelium determines Ca2+ channel availability in smooth muscle:: involvement of nitric oxide
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DOI：
10.1007/s004240051001
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发表时间：
2000-04-01
影响因子：
4.5
通讯作者：
Li, X
中科院分区：
文献类型：
--
作者：
Simard, JM;Li, X
内皮细胞通过一氧化氮（NO）调节平滑肌收缩力。我们测试了内皮功能障碍的假设，无论是由损伤产生的，还是通过降低NO的生物利用度的药理学模拟，都会导致从血管分离的平滑肌细胞中Ca2+通道可用性升高（ng,,,,=最大电导/细胞电容）。在正常血压的Wistar大鼠基底动脉中，我们测量了对照血管、用氟化钠加光损伤内皮的血管和用NO清除剂1h -咪唑-1-基氧基，2-（4-羧基苯基）-4,5-二氢-4,4,5,5-四甲基-3-氧化物钾盐（C-PTIO）预处理降低NO生物利用度的血管的平滑肌细胞的ng…或内皮型一氧化氮合酶（eNOS）抑制剂ng -硝基- l -精氨酸甲酯（L-NAME）。四组细胞的ng…值分别为0.28+/-0.02 nS/pF （n=22）、0.51+/-0.05 nS/pF （n=15）、0.43+/-0.03 nS/pF （n=12）和0.47+/-0.04 nS/pF （n=14）
Endothelium regulates smooth muscle contractility in part via nitric oxide (NO). We tested the hypothesis that endothelial dysfunction, either produced by injury or simulated pharmacologically by reducing the bioavailability of NO, results in elevated Ca2+ channel availability (ng,,,,= maximum conductance/cell capacitance) in smooth muscle cells isolated from the vessel. Using basilar arteries of normotensive Wistar rats, we measured ng,,, in smooth muscle cells from control vessels, from vessels in which endothelium was injured using Na fluoroscene plus light, and from vessels in which the bioavailability of NO was reduced by pretreatment with the NO scavenger 1H-imidazol-1-yloxy,2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-3-oxide,potassium salt (C-PTIO), or the endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Values of ng,,, in these four groups of cells were 0.28+/-0.02 nS/pF (n=22), 0.51+/-0.05 nS/pF (n=15), 0.43+/-0.03 nS/pF (n=12), and 0.47+/-0.04 nS/pF (n=14) (P