Liu J L, Murakami H, Zucker I H
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575, USA.
Am J Physiol. 1996 Jun;270(6 Pt 2):R1361-70. doi: 10.1152/ajpregu.1996.270.6.R1361.
Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.
近期数据表明，一氧化氮（NO）在交感神经活动和压力反射敏感性的调节中发挥作用。这些研究大多在麻醉状态的实验动物身上进行，对于NO在心率和交感神经活动的压力反射控制中的相对作用，几乎没有进行过比较。在本研究中，我们在清醒的、已植入仪器的家兔身上，研究了NO合酶抑制剂NG-硝基-L-精氨酸（L-NNA）对心率（HR）和肾交感神经活动（RSNA）的压力反射控制的影响。静脉推注13mg/kg的L-NNA可降低基础心率（从205.0±6.0降至145.5±8.2次/分钟；P<0.05），而平均动脉压（MAP）和RSNA无显著变化。L-NNA显著降低了HR-MAP曲线的较低平台期，并增加了HR和RSNA的压力反射控制敏感性。L-精氨酸（600mg/kg静脉注射）而非D-精氨酸可逆转上述效应。L-NNA对基础心率的影响未被美托洛尔（2mg/kg）或阿托品（0.2mg/kg）完全阻断。在用美托洛尔预处理后，压力反射敏感性降低，而L-NNA使压力反射敏感性恢复到对照水平。在用阿托品预处理后，L-NNA仍降低较低平台期，但对压力反射敏感性无显著影响。在水合氯醛麻醉、去窦弓神经（SAD）的家兔中，L-NNA增加了对主动脉神经电刺激的心率反应，但未增加RSNA反应。L-NNA对右迷走神经刺激的心率反应无影响。在清醒完整和SAD家兔中，L-NNA均未增加基础RSNA。这些结果表明，内源性NO降低了HR和RSNA的压力反射控制。交感和副交感成分在NO对HR压力反射控制的作用中均发挥作用。NO在中枢神经系统中的作用在HR的压力反射控制中比在RSNA的压力反射控制中更为重要。
