Pressor reflex evoked by static muscle contraction: role of nitric oxide in the dorsal horn.
Pressor reflex evoked by static muscle contraction: role of nitric oxide in the dorsal horn.
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静态肌肉收缩引起的升压反射：一氧化氮在背角的作用。
DOI：
10.1152/ajpregu.1999.276.6.r1639
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Crews,AD
中科院分区：
文献类型：
--
作者：
Wilson,LB;Engbretson,J;Crews,AD
在这项研究中，我们测试的假设，一氧化氮（NO）的生产在背角参与产生升压反射引起的骨骼肌静态收缩。用α-氯醛糖（80 mg/kg）和乌拉坦（100 mg/kg）麻醉猫，并进行椎板切除术。除L7背根外，另一侧切断L5 ~ S2背根和前根，电刺激L7和S1前根外周端，诱发同侧小腿三头肌的静态收缩。在L 6和S1脊髓背角注射NO合成酶抑制剂NG-硝基-L-精氨酸甲酯（50 mmol/l注射浓度，基于剂量-反应数据），不能减弱静态收缩引起的平均动脉压（MAP）的峰值变化（ΔMAP，mmHg，注射NAME前：57 ± 5，注射NAME 2 h后：50 ± 6）。然而，当收缩10 s时的MAP从27 ± 4 mmHg降至17 ± 4 mmHg时，这种fl-NAME透析降低了初始升压反应的幅度。另一方面，50 mmol/l精氨酸透析2 h使代表升压反应时程的曲线上移，使静态收缩的峰值升压反应从51 ± 9 mmHg增加到68 ± 9 mmHg。d-NAME（50 mmol/l）透析2 h对时间进程或峰值升压反应无影响（ΔMAP（mmHg）：透析前为78 ± 12，透析后为72 ± 15）。这些数据表明，NO的产生在背角有调节作用的升压反射引起的骨骼肌静态收缩和增加NO的水平在背角增强背角细胞的兴奋性肌肉传入输入。
In this study, we tested the hypothesis that nitric oxide (NO) production in the dorsal horn is involved in producing the pressor reflex elicited by static contraction of skeletal muscle. Cats were anesthetized with α-chloralose (80 mg/kg) and urethane (100 mg/kg), and a laminectomy was performed. With the exception of the L7dorsal root, the dorsal and ventral roots from L5to S2were sectioned on one side and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L7and S1ventral roots. Dialysis of the NO synthase inhibitorNG-nitro-l-arginine methyl ester (l-NAME; 50 mmol/l syringe concentration, based upon dose-response data) into the dorsal horn at L6and S1failed to attenuate the peak change in mean arterial pressure (MAP) evoked by static contraction (ΔMAP in mmHg: 57 ± 5 before and 50 ± 6 after 2 h ofl-NAME). However, this dialysis ofl-NAME reduced the magnitude of the initial pressor response as the MAP at 10 s of the contraction fell from 27 ± 4 to 17 ± 4 mmHg. On the other hand, 2 h ofl-arginine dialysis (50 mmol/l) shifted the curve representing the time course of the pressor response upward and increased the peak pressor response to static contraction from 51 ± 9 to 68 ± 9 mmHg. A 2-h dialysis ofd-NAME (50 mmol/l), the inactive enantiomer ofl-NAME, had no effect on the time course or the peak pressor response (ΔMAP in mmHg: 78 ± 12 before and 72 ± 15 after). These data suggest that NO production in the dorsal horn has a modulatory influence on the pressor reflex evoked by static contraction of skeletal muscle and that increasing the level of NO in the dorsal horn enhances the excitability of dorsal horn cells to muscle afferent input.