Nitric oxide inhibits norepinephrine stimulated contraction of human internal thoracic artery and rat aorta.

Nitric oxide inhibits norepinephrine stimulated contraction of human internal thoracic artery and rat aorta.
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一氧化氮抑制去甲肾上腺素刺激的人胸内动脉和大鼠主动脉的收缩。

DOI:
10.1006/phrs.2000.0765
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发表时间:
2001
影响因子:
9.3
通讯作者:
Magazine,HI
Magazine,HI
中科院分区:
医学1区
文献类型:
--
作者:
Stefano,GB;Murga,J;Benson,H;Zhu,W;Bilfinger,TV;Magazine,HI

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采用大鼠主动脉和人胸廓内动脉(ITA)及NO供体SNAP,研究了一氧化氮(NO)对去甲肾上腺素(NE)诱导的血管收缩的影响。使用安培探针直接测量NO水平。需要大于2nM的NO浓度来减少由100 nM去甲肾上腺素(NE)诱导的血管收缩。在NE添加之前或之后将主动脉环暴露于SNAP,导致NE诱导的收缩的类似衰减。与此相反,增加的ITA段响应SNAP的松弛观察到相对于大鼠主动脉和NE添加后的收缩张力的显着发展没有观察到。细胞骨架肌动蛋白的评价表明,在平滑肌细胞中的F-肌动蛋白含量显着损失后,NO暴露,这表明NO可能有直接和间接的影响收缩张力。这些数据一起表明,血管收缩剂的反应性可能会显着衰减事先或随后暴露于NO,和机制,除了血管舒张可能有助于这种效果。
The effect of nitric oxide (NO) on norepinephrine-induced vascular contraction was evaluated using segments of rat aorta and human internal thoracic artery (ITA) and the NO donor, SNAP. NO levels were measured directly using an amperometric probe. Concentrations of NO greater than 2 nM were required to reduce vascular contraction induced by 100 nM norepinephrine (NE). Exposure of the aortic rings to SNAP prior to, or after NE addition, resulted in a similar attenuation of NE-induced contraction. In contrast, increased relaxation of ITA segments in response to SNAP was observed relative to that of rat aorta and significant development of contractile tone following NE addition was not observed. Evaluation of cytoskeletal actin demonstrated marked loss of F-actin content in smooth muscle cells following NO exposure, suggesting that NO may have direct and indirect effects on contractile tone. These data taken together suggest that vascular responsiveness to contractile agents may be significantly attenuated by prior or subsequent exposure to NO, and mechanisms in addition to vascular relaxation are likely to contribute to this effect.
当单核细胞或巨噬细胞存在时,内皮素-1 的血管收缩能力会增强。
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