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一氧化氮的生理性释放取决于血管张力水平。

Physiological release of nitric oxide is dependent on the level of vascular tone.

作者信息

Vargas H M, Ignarro L J, Chaudhuri G

机构信息

Department of Pharmacology, UCLA-School of Medicine 90024-1735.

出版信息

Eur J Pharmacol. 1990 Nov 13;190(3):393-7. doi: 10.1016/0014-2999(90)94204-b.

Abstract

The pressor effect of NG-methyl-L-arginine (NMA) was tested in urethane-anesthetized rats which were untreated (control) or devoid of sympathetic tone. In contrast with controls, the NMA response was attenuated by pithing or ganglionic blockade. In pithed rats, the induction of moderate or intense vasoconstriction with constant phenylephrine infusion restored or augmented, respectively, the NMA pressor response. Our data suggest that vascular tone may physiologically regulate the release of nitric oxide in vivo.

摘要

在未处理(对照)或失去交感神经张力的氨基甲酸乙酯麻醉大鼠中测试了NG-甲基-L-精氨酸(NMA)的升压作用。与对照组相比,NMA反应因脊髓损毁或神经节阻断而减弱。在脊髓损毁的大鼠中,持续输注去氧肾上腺素诱导中度或强烈血管收缩分别恢复或增强了NMA升压反应。我们的数据表明,血管张力可能在生理上调节体内一氧化氮的释放。

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