Nitric oxide mediates cat hindlimb cholinergic vasodilation induced by stimulation of posterior hypothalamus.
Nitric oxide mediates cat hindlimb cholinergic vasodilation induced by stimulation of posterior hypothalamus.
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一氧化氮介导刺激下丘脑后部引起的猫后肢胆碱能血管舒张。
DOI：
10.2170/jjphysiol.43.473
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Ishio Ninomiya
中科院分区：
文献类型：
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作者：
Kanji Matsukawa;T. Shindo;Mikiyasu Shirai;Ishio Ninomiya
这项工作的目的是检查内皮源性舒张因子（一氧化氮）是否介导下丘脑后部刺激引起的猫后肢胆碱能血管舒张和静脉注射引起的β-肾上腺素能血管舒张。使用一氧化氮合成抑制剂 NW-硝基-L-精氨酸甲酯 (L-NAME) 注射异丙肾上腺素。没有 L-NAME 时，下丘脑刺激期间股骨血流速度 (FBV) 从基线值 8.4 +/- 2.2 cm/s 增加 11.2 +/- 2.2 cm/s（平均值 +/- SEM），股骨电导 (FC) 从 0.062 +/- 0.016 增加 0.084 +/- 0.021 cm/s/mmHg cm/s/mmHg，被阿托品（0.5 mg I.A.）消除。下丘脑刺激（15 +/- 8 mmHg 和 22 +/- 6 次/分钟）期间动脉血压 (AP) 和心率 (HR) 增加。当注射异丙肾上腺素（1-2微克静脉注射）时，FBV和FC增加5.1+/-0.56cm/s和0.048+/-0.005cm/s/mmHg。使用 L-NAME（20-100 mg I.A.），下丘脑刺激期间 AP 和 HR 的升高没有变化，但 FBV 和 FC 的升高显着减弱至 5.2 +/- 3.7 cm/s 和 0.026 +/- 0.021 cm/s/mmHg。相比之下，L-NAME 不影响 FBV 和 FC 在刺激 β-肾上腺素能受体期间的反应。 NG-单甲基-L-精氨酸（10-30 mg I.A.）的效果与 L-NAME 相同。表明一氧化氮参与下丘脑刺激神经诱导的后肢胆碱能血管舒张，但不参与β-肾上腺素能血管舒张。
The aim of this work was to examine whether endothelium-derived relaxing factor (nitric oxide) mediates cat hindlimb cholinergic vasodilation induced by stimulation of the posterior hypothalamus and beta-adrenergic vasodilation by I.V. injection of isoproterenol using an inhibitor of nitric oxide synthesis, NW-nitro-L-arginine methyl ester (L-NAME). Without L-NAME, femoral blood flow velocity (FBV) increased during hypothalamic stimulation by 11.2 +/- 2.2 cm/s (mean +/- SEM) from the baseline value of 8.4 +/- 2.2 cm/s and femoral conductance (FC) increased by 0.084 +/- 0.021 cm/s/mmHg from 0.062 +/- 0.016 cm/s/mmHg, which were abolished by atropine (0.5 mg I.A.). Arterial blood pressure (AP) and heart rate (HR) increased during hypothalamic stimulation (15 +/- 8 mmHg and 22 +/- 6 beats/min). When isoproterenol (1-2 micrograms I.V.) was injected, FBV and FC increased 5.1 +/- 0.56 cm/s and 0.048 +/- 0.005 cm/s/mmHg. With L-NAME (20-100 mg I.A.), the rises in AP and HR during hypothalamic stimulation were unchanged but the increases in FBV and FC were significantly blunted to 5.2 +/- 3.7 cm/s and 0.026 +/- 0.021 cm/s/mmHg. In contrast, L-NAME did not affect the responses in FBV and FC during stimulation of beta-adrenergic receptors. The effect of NG-monomethyl-L-arginine (10-30 mg I.A.) was the same as L-NAME. It is suggested that nitric oxide is involved in hindlimb cholinergic vasodilation neurally induced by hypothalamic stimulation but not in beta-adrenergic vasodilation.