Kellogg D L, Pérgola P E, Piest K L, Kosiba W A, Crandall C G, Grossmann M, Johnson J M
Department of Medicine, University of Texas Health Science Center at San Antonio 78284, USA.
Circ Res. 1995 Dec;77(6):1222-8. doi: 10.1161/01.res.77.6.1222.
During heat stress, increases in blood flow in nonglabrous skin in humans are mediated through active vasodilation by an unknown neurotransmitter mechanism. To investigate this mechanism, a three-part study was performed to determine the following: (1) Is muscarinic receptor activation necessary for active cutaneous vasodilation? We iontophoretically applied atropine to a small area of forearm skin. At that site and an untreated control site, we measured the vasomotor (laser-Doppler blood flow [LDF]) and sudomotor (relative humidity) responses to whole-body heat stress. Blood pressure was monitored. Cutaneous vascular conductance (CVC) was calculated (LDF divided by mean arterial pressure). Sweating was blocked at treated sites only. CVC rose at both sites (P < .05 at each site); thus, cutaneous active vasodilation is not effected through muscarinic receptors. (2) Are nonmuscarinic cholinergic receptors present on cutaneous arterioles? Acetylcholine (ACh) was iontophoretically applied to forearm skin at sites pretreated by atropine iontophoresis and at untreated sites. ACh increased CVC at untreated sites (P < .05) but not at atropinized sites. Thus, the only functional cholinergic receptors on cutaneous vessels are muscarinic. (3) Does cutaneous active vasodilation involve cholinergic nerve cotransmission? Botulinum toxin was injected intradermally in the forearm to block release of ACh and any coreleased neurotransmitters. Heat stress was performed as in part 1 of the study. At treated sites, CVC and relative humidity remained at baseline levels during heat stress (P > .05). Active vasodilator and sudomotor responses to heat stress were abolished by botulinum toxin. We conclude that cholinergic nerve activation mediates cutaneous active vasodilation through release of an unknown cotransmitter, not through ACh.
在热应激期间，人类无毛皮肤的血流量增加是通过一种未知的神经递质机制介导的主动血管舒张实现的。为了研究这一机制，我们进行了一项分为三个部分的研究，以确定以下内容：（1）毒蕈碱受体激活对于主动皮肤血管舒张是否必要？我们通过离子电渗法将阿托品应用于前臂皮肤的一小片区域。在该部位和未处理的对照部位，我们测量了对全身热应激的血管舒缩（激光多普勒血流 [LDF]）和发汗运动（相对湿度）反应。监测血压。计算皮肤血管传导率（CVC）（LDF 除以平均动脉压）。仅在处理部位出汗被阻断。两个部位的 CVC 均升高（每个部位 P < .05）；因此，皮肤主动血管舒张不是通过毒蕈碱受体实现的。（2）皮肤小动脉上是否存在非毒蕈碱胆碱能受体？通过离子电渗法将乙酰胆碱（ACh）应用于经阿托品离子电渗预处理的部位和未处理的前臂皮肤部位。ACh 在未处理部位增加了 CVC（P < .05），但在阿托品处理部位没有增加。因此，皮肤血管上唯一有功能的胆碱能受体是毒蕈碱受体。（3）皮肤主动血管舒张是否涉及胆碱能神经共同传递？将肉毒杆菌毒素皮内注射到前臂以阻断 ACh 和任何共释放神经递质的释放。如研究的第 1 部分那样进行热应激。在处理部位，热应激期间 CVC 和相对湿度保持在基线水平（P > .05）。肉毒杆菌毒素消除了对热应激的主动血管舒张和发汗运动反应。我们得出结论，胆碱能神经激活通过释放一种未知的共递质而非 ACh 介导皮肤主动血管舒张。
