The involvement of nitric oxide in the cutaneous vasoconstrictor response to local cooling in humans
The involvement of nitric oxide in the cutaneous vasoconstrictor response to local cooling in humans
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DOI：
10.1113/jphysiol.2006.109884
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发表时间：
2006-08-01
影响因子：
5.5
通讯作者：
Johnson, John M.
中科院分区：
文献类型：
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作者：
Hodges, Gary J.;Zhao, Kun;Johnson, John M.
局部降温(LC)使皮肤血管传导性(CVC)下降。先前的工作表明，LC的血管收缩反应的至少一部分可能是通过抑制一氧化氮合酶(NOS)的活性来实现的。在这项研究中，我们进一步测试了这一概念。共8名受试者(男6名，女2名)(第一部分n=7；第二部分n=5，其中4人参与第一部分)。用激光多普勒血流仪监测皮肤血流量。局部皮肤和体温的控制分别通过佩尔蒂埃冷热探针架和浸水套装实现。微透析纤维在无菌情况下插入。微透析法分别注入生理盐水、L-NAME(20 mM，用于抑制一氧化氮合酶活性)和硝普钠(SNP，10亩M)。用离子导入法给药，阻断肾上腺素能功能。根据血流量和血压计算CVC。第一部分旨在确定NO和肾上腺素能系统的相对作用。注射L后，L名和BT+L名两个部位的CVC分别下降了35+/-4%(P<；0.05)，慢速LC(34-24℃)35分钟后，对照部位(68+/-4%)和BT治疗部位(39+/-5%)的CVC均显著下降(P<；0.05)。在L名字处理的部位，LC导致CVC进一步下降23+/-5%(P<；0.05)。重要的是，LC对BT+L名字部位的CVC没有影响(P>；0.05)。第二部分的目的是测试LC的影响是否特定于NOS酶。两个站点同时进行了BT和L-NAME的预处理。50min后，加入SNP作为NO供体，在一个部位恢复基线CVC。应用了与第1部分相同的LC过程。在基础CVC恢复的部位，CVC下降了24+/-10%(P<；0.05)，而在只接受BT+L-NAME治疗的部位，CVC没有变化(P>；0.05)。这些数据表明，慢LC的血管收缩是由于去甲肾上腺素释放增加和一氧化氮合酶本身及其下游突起活性降低所致。
Cutaneous vascular conductance (CVC) declines in response to local cooling (LC). Previous work indicates that at least part of the vasoconstrictor response to LC may be through an inhibitory effect on nitric oxide synthase (NOS) activity. In this study we further tested that notion. A total of eight (6 male, 2 female) subjects participated (Part 1 n= 7; Part 2 n= 5, 4 of whom participated in Part 1). Skin blood flow was monitored by laser-Doppler flowmetry. Control of local skin and body temperatures was achieved with Peltier cooler/heater probe holders and water perfused suits, respectively. Microdialysis fibres were inserted aseptically. Saline, L-NAME (20 mM; to inhibit NOS activity) and sodium nitroprusside (SNP 10 mu M) were infused by microdialysis. Bretylium tosylate (BT), to block adrenergic function, was administered by iontophoresis. CVC was calculated from blood flow and blood pressure. Part 1 was designed to determine the relative roles of the NO and the adrenergic systems. The infusion of L-NAME elicited a 35 +/- 4% decrease in CVC at the L-NAME and BT + L-NAME sites (P < 0.05); subsequent slow LC (34-24 degrees C) for 35 min caused a significant (P < 0.05) decrease in CVC at control sites (68 +/- 4%) and at the BT treated sites (39 +/- 5%). LC caused a further 23 +/- 5% of initial baseline decrease in CVC at the L-NAME treated sites (P < 0.05). Importantly, CVC at the BT + L-NAME sites was unaffected by LC (P > 0.05). Part 2 was designed to test whether LC influences were specific to the NOS enzymes. Two sites were pretreated with both BT and L-NAME. After 50 min, SNP was added as an NO donor to restore baseline CVC at one site. The same LC process as in Part 1 was applied. There was a 24 +/- 10% decrease (P < 0.05) in CVC at sites with baseline CVC restored, while, as in Part 1, there was no change (P > 0.05) at sites treated with BT + L-NAME only. These data suggest that the vasoconstriction with slow LC is due to a combination of increased noradrenaline release and decreased activity of both NOS per se and of process(es) downstream of NOS.