ELEVATED SYMPATHETIC-NERVE ACTIVITY IN BORDERLINE HYPERTENSIVE HUMANS - EVIDENCE FROM DIRECT INTRANEURAL RECORDINGS
ELEVATED SYMPATHETIC-NERVE ACTIVITY IN BORDERLINE HYPERTENSIVE HUMANS - EVIDENCE FROM DIRECT INTRANEURAL RECORDINGS
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DOI：
10.1161/01.hyp.14.2.177
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发表时间：
1989-08-01
期刊：
影响因子：
8.3
通讯作者：
MARK, AL
中科院分区：
文献类型：
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作者：
ANDERSON, EA;SINKEY, CA;MARK, AL
有关血浆儿茶酚胺水平升高和对自主神经阻断的增强反应的报告表明交感神经张力在交感神经紧张中升高。目前尚不清楚这是否反映了更多的交感神经外流。我们直接记录了15名血压正常和12名临界高血压年龄匹配的男性的肌交感神经活动(显微神经学)，以确定临界高血压患者的交感神经活性是否升高。分别测定低钠和高钠饮食(10和400meq钠/24小时)6天后的仰卧心率、血压、血浆去甲肾上腺素和传出肌交感神经活动(腓神经)。交感神经活性在交感神经活性和交感神经活性这两个低(37。临界性高血压患者1例，+-29例。血压正常组为1次/分钟；临界高血压组为25+1次/分钟；临界高血压组为16.+-次/分钟。在血压正常的人中为1次/分钟；钠饮食。临界高血压组有更高的收缩压(p<；0.01)和舒张压(p<；0.05)，与钠摄入量无关。在两组中，高钠摄入降低了乳交感神经活性(p<；0.001)、血浆去甲肾上腺素(p<；0.001)、舒张压(p<；0.02)、心率(p<；0.002)和体重增加(p<；0.05)。观察到血浆去甲肾上腺素水平存在显著的(p<；0.05)逐组饮食交互作用。与正常血压组相比，临界高血压组低钠饮食时血浆去甲肾上腺素水平升高(p=0.8)，高钠饮食时去甲肾上腺素水平降低(p=0.23)。高钠摄入量使27名受试者(4名临界高血压患者和2名正常血压患者)中6名患者的舒张压升高超过5毫米汞柱。与钠抵抗受试者相比，钠敏感受试者的交感神经活性并没有升高，而且在高钠摄入量时也有所下降。本研究支持Broderline高血压中枢交感神经流出增加的假说。
Reports of elevated plasma catecholamine levels and augmented responses to autonomic blockade suggest increased sympathetic tone in borderline hypertension. It is not known if this reflects greater sympathetic neural outflow. We directly recorded muscle sympathetic nerve activity (microneurography) in 15 normotensive and 12 borderline hypertensive age-matched men to determine whether borderline hypertensive individuals have elevated sympathetic nerve activity. Supine heart rate, blood pressure, plasma norepinephrine, and efferent muscle sympathetic nerve activity (peroneal nerve) was measured after 6 days of both low and high dietary sodium intake (10 and 400 meq sodium/24 hr). Sympathetic nerve activity was elevated significantly in borderline hypertensive individuals on both low (37 .+-. 1 in borderline hypertensive individuals vs. 29 .+-. 1 bursts/min in normotensive individuals; p < 0.01) and high (25 + 1 in borderline hypertensive individuals vs. 16 .+-. 1 bursts/min in normotensive individuals; p < 0.01) sodium diets. The borderline hypertensive group had higher systolic (p < 0.01) and diastolic (p < 0.05) blood pressures independent of sodium intake. Across both groups, high sodium intake reduced msucle sympathetic nerve activity (p < 0.001), plasma norepinephrine (p < 0.001), diastolic blood pressure (p < 0.02), heart rate (p < 0.002), and increased weight (p < 0.05). A significant (p < 0.05) group-by-diet interaction was observed for plasma norepinephrine levels. Specifically, compared with the normotensive group, plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet (p = 0.8) and lower on high sodium diet (p = 0.23). High sodium intake increased diastolic pressure by over 5 mm Hg in six on 27 subject (four borderline hypertensive and two normotensive). Sympathetic activity in sodium-sensitive subjects was not elevated compared with sodium-resistant subjects and also declined during high sodium intake. This study supports the hypothesis of elevated central sympathetic neural outflow in broderline hypertension.