HYPERINSULINEMIA PRODUCES BOTH SYMPATHETIC NEURAL ACTIVATION AND VASODILATION IN NORMAL HUMANS
HYPERINSULINEMIA PRODUCES BOTH SYMPATHETIC NEURAL ACTIVATION AND VASODILATION IN NORMAL HUMANS
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DOI：
10.1172/jci115260
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发表时间：
1991-06-01
影响因子：
15.9
通讯作者：
MARK, AL
中科院分区：
文献类型：
--
作者：
ANDERSON, EA;HOFFMAN, RP;MARK, AL
高胰岛素血症可能通过增加交感神经活性和血管阻力而导致高血压。 我们试图确定胰岛素是否增加人类中枢交感神经流出和血管阻力。 我们记录了肌肉交感神经活动（MSNA;微神经，腓神经），前臂血流量（体积描记法），心率和血压在14名血压正常的男性在1小时的低（38 mU/m2/min）和高（76 mU/m2/min）剂量的胰岛素输注，同时保持血糖恒定。 血浆胰岛素从对照期间的8 +/- 1-mu-U/ml分别上升到低和高胰岛素剂量期间的72 +/- 8和144 +/- 13-mu-U/ml，并且在胰岛素输注停止后1小时下降到15 +/- 6-mu-U/ml。 MSNA在对照组中平均为21.5 +/- 1.5爆发/分钟，在低剂量和高剂量胰岛素（分别为+/- 5.4和+/- 9.3爆发/分钟）期间显著增加（P < 0.001），并在1小时恢复期间进一步增加（+ 15.2爆发/分钟）。 血浆去甲肾上腺素水平（对照组为119 +/- 19 pg/ml）在低剂量（258 +/- 25; P < 0.02）和高剂量（285 +/- 95; P < 0.01）胰岛素和恢复期（316 +/- 23; P < 0.01）均升高。 胰岛素输注期间血浆肾上腺素水平未发生变化。 尽管MSNA和血浆去甲肾上腺素增加，但在两种剂量的胰岛素期间，前臂血流量显著增加（P < 0.001），前臂血管阻力降低。 输注胰岛素前后收缩压无明显变化，舒张压下降4-5 mmHg（P < 0.01）。 这项研究表明，急性增加血浆胰岛素在生理范围内提高交感神经流出，但产生前臂血管舒张，不升高正常人的动脉压。
Hyperinsulinemia may contribute to hypertension by increasing sympathetic activity and vascular resistance. We sought to determine if insulin increases central sympathetic neural out-flow and vascular resistance in humans. We recorded muscle sympathetic nerve activity (MSNA; microneurography, peroneal nerve), forearm blood flow (plethysmography), heart rate, and blood pressure in 14 normotensive males during 1-h infusions of low (38 mU/m2/min) and high (76 mU/m2/min) doses of insulin while holding blood glucose constant. Plasma insulin rose from 8 +/- 1-mu-U/ml during control, to 72 +/- 8 and 144 +/- 13-mu-U/ml during the low and high insulin doses, respectively, and fell to 15 +/- 6-mu-U/ml 1 h after insulin infusion was stopped. MSNA, which averaged 21.5 +/- 1.5 bursts/min in control, increased significantly (P < 0.001) during both the low and high doses of insulin (+/- 5.4 and +/- 9.3 bursts/min, respectively) and further increased during 1-h recovery (+ 15.2 bursts/min). Plasma norepinephrine levels (119 +/- 19 pg/ml during control) rose during both low (258 +/- 25; P < 0.02) and high (285 +/- 95; P < 0.01) doses of insulin and recovery (316 +/- 23; P < 0.01). Plasma epinephrine levels did not change during insulin infusion. Despite the increased MSNA and plasma norepinephrine, there were significant (P < 0.001) increases in forearm blood flow and decreases in forearm vascular resistance during both doses of insulin. Systolic pressure did not change significantly during infusion of insulin and diastolic pressure fell approximately 4-5 mmHg (P < 0.01). This study suggests that acute increases in plasma insulin within the physiological range elevate sympathetic neural outflow but produce forearm vasodilation and do not elevate arterial pressure in normal humans.