Role of nitric oxide in methacholine-induced sweating and vasodilation in human skin
Role of nitric oxide in methacholine-induced sweating and vasodilation in human skin
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DOI：
10.1152/japplphysiol.00122.2005
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发表时间：
2006-04-01
影响因子：
3.3
通讯作者：
Mack, GW
中科院分区：
文献类型：
--
作者：
Lee, K;Mack, GW
本研究的目的是确定一氧化氮合酶抑制剂 N-G-硝基-L-精氨酸甲酯 (L-NAME) 在乙酰甲胆碱 (MCh) 刺激的人前臂皮肤出汗过程中是否表现出显着的毒蕈碱受体拮抗作用。将三个皮内微透析探针放置在八名健康成年人（4 名男性和 4 名女性）的皮肤中。在存在或不存在一氧化氮合酶抑制剂 L-NAME (10 mM) 或 L-精氨酸类似物 N-G-单甲基-L-精氨酸 (L-NMMA; 10 mM) 的情况下，通过微透析探针分九个步骤灌注 0.033-243 mM 范围内的 MCh。直接在每个微透析探针上测量局部出汗率（出汗率）和皮肤血流量（激光多普勒测速法）。我们观察到仅 MCh、MCh 和 L-NAME、MCh 和 L-NMMA 部位的静息出汗率相似，平均分别为 0.175 +/- 0.029、0.186 +/- 0.034 和 0.139 +/- 0.027 mg center dot min(-1) center dot cm (-2)。所有三个位点的峰值出汗率（0.46 +/- 0.11、0.56 +/- 0.16 和 0.53 +/- 0.16 mg 中心点 min(-1) 中心点 cm(-2)）也相似。 MCh 产生 S 形剂量反应曲线，并且在 L-NAME 或 L-NMMA 存在的情况下，最大可达到反应的 50%（仅限 MCh 为 0.42 +/- 0.14 mM）向右移动（分别为 2.88 +/- 0.79 和 3.91 +/- 1.14 mM；P < 0.05）。这些结果表明，一氧化氮可以增强人体皮肤中 MCh 刺激的汗腺功能。此外，L-NAME 始终减弱 MCh 诱导的血管舒张，而 L-NMMA 则不然。这些数据支持这样的假设：毒蕈碱诱导的皮肤血管扩张不是由一氧化氮的产生介导的，并且 L-NAME 在减弱乙酰胆碱诱导的血管舒张中的作用可能是由于其作为毒蕈碱受体拮抗剂的潜力。
The purpose of this study was to determine whether the nitric oxide synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) demonstrates significant muscarinic-receptor antagonism during methacholine (MCh)-stimulated sweating in human forearm skin. Three intradermal microdialysis probes were placed in the skin of eight healthy adults ( 4 men and 4 women). MCh in the range of 0.033-243 mM in nine steps was perfused through a microdialysis probe with and without the presence of the nitric oxide synthase inhibitor L-NAME ( 10 mM) or the L-arginine analog N-G-monomethyl-L-arginine (L-NMMA; 10 mM). Local sweat rate ( sweat rate) and skin blood flow (laser-Doppler velocimetry) were measured directly over each microdialysis probe. We observed similar resting sweat rates at MCh only, MCh and L-NAME, and MCh and L-NMMA sites averaging 0.175 +/- 0.029, 0.186 +/- 0.034, and 0.139 +/- 0.027 mg center dot min(-1) center dot cm (-2), respectively. Peak sweat rate (0.46 +/- 0.11, 0.56 +/- 0.16, and 0.53 +/- 0.16. mg center dot min(-1) center dot cm(-2)) was also similar among all three sites. MCh produced a sigmoid-shape dose-response curve and 50% of the maximal attainable response (0.42 +/- 0.14 mM for MCh only) was shifted rightward shift in the presence of L-NAME or L-NMMA (2.88 +/- 0.79 and 3.91 +/- 1.14 mM, respectively; P < 0.05). These results indicate that nitric oxide acts to augment MCh-stimulated sweat gland function in human skin. In addition, L-NAME consistently blunted the MCh-induced vasodilation, whereas L-NMMA did not. These data support the hypothesis that muscarinic-induced dilation in cutaneous blood vessels is not mediated by nitric oxide production and that the role of L-NAME in attenuating acetylcholine-induced vasodilation may be due to its potential to act as a muscarinic-receptor antagonist.