Basilar arterial construction caused by intracisternal NG-nitro-L-arginine in anesthetized monkeys.
Basilar arterial construction caused by intracisternal NG-nitro-L-arginine in anesthetized monkeys.
复制标题
麻醉猴脑池内 NG-硝基-L-精氨酸引起的基底动脉构建。
DOI：
10.1016/s0008-6363(95)00077-1
复制
发表时间：
1995
影响因子：
10.8
通讯作者：
N. Toda
中科院分区：
文献类型：
--
作者：
T. Okamura;K. Ayajiki;N. Toda
目的：本研究旨在确定紧张性一氧化氮（NO）介导的血管扩张神经支配是否参与麻醉日本猴基底动脉扩张。方法：血管造影测量基底动脉直径，脑池内应用一氧化氮合酶抑制剂NG-硝基-L-精氨酸（l-NNA）。结果：注射l-NNA可引起基底动脉持续收缩，其作用可被脑池内注射l-精氨酸逆转。酚妥拉明有加速血管收缩的趋势。在α-肾上腺素能受体阻断下，六甲铵显著减弱对NNA的缩血管反应。脑池内注射这种抑制剂并没有改变全身血压和心率。结论：这些研究结果表明，猴子基底动脉的NO合成酶抑制剂的收缩与抑制NO的合成在血管扩张神经接受紧张性冲动从中枢神经系统。在麻醉猴中，基底动脉张力似乎受到一氧化氮能和肾上腺素能神经以及来自内皮的NO的调节。
Objectives:The present study was designed to determine whether tonic nitric oxide (NO)-mediated vasodilator innervation participates in basilar arterial dilatation in the anesthetized Japanese monkey.Methods:The basilar arterial diameter was angiographically measured, andNG-nitro-l-arginine (l-NNA), a nitric oxide synthase inhibitor, was intracistemally applied.Results:The injection ofl-NNA produced a sustained constriction of the basilar artery, the effect being reversed by the cisternal injection ofl-arginine. The vasoconstriction tended to be accelerated by treatment with phentolamine. Under α-adrenoceptor blockade, hexamethonium significantly attenuated the vasoconstrictor response tol-NNA. Intracisternal injections of this inhibitor did not alter the systemic blood pressure and heart rate.Conclusions:These findings suggest that constriction by the NO synthase inhibitor of the monkey basilar artery is associated with suppression of synthesis of NO in vasodilator nerves receiving tonic impulses from the central nervous system. The basilar arterial tone appears to be regulated by nitroxidergic and adrenergic nerves and by NO derived from the endothelium in anesthetized monkeys.