Low P A, Opfer-Gehrking T L, Kihara M
Department of Neurology, Mayo Foundation, Rochester, MN 55905.
Clin Auton Res. 1992 Feb;2(1):29-34. doi: 10.1007/BF01824208.
The receptor pharmacology of the human sweat gland was studied in vivo. The axon-reflex response was mediated by nicotinic receptors which were activated by nicotine and acetylcholine, but not pilocarpine, and inhibited by hexamethonium. The direct response was mainly muscarinic, responding to pilocarpine and acetylcholine. A component of the direct response was nicotinic, since it was activated by nicotine and blocked by hexamethonium in a dose-dependent manner. The axon-reflex response to nicotine and acetylcholine was partially blocked by pilocarpine, especially when application of pilocarpine preceded the procedure. The inhibition of the nicotinic response may be secondary to M1 antagonism since pilocarpine is an M2 agonist and M1 antagonist and pirenzepine, a specific M1 antagonist, caused similar effects as pilocarpine.
对人体汗腺的受体药理学进行了体内研究。轴突反射反应由烟碱受体介导，烟碱和乙酰胆碱可激活该受体，但毛果芸香碱不能激活，六甲铵可抑制该受体。直接反应主要是毒蕈碱样的，对毛果芸香碱和乙酰胆碱有反应。直接反应的一个成分是烟碱样的，因为它可被烟碱激活，并被六甲铵以剂量依赖的方式阻断。毛果芸香碱可部分阻断对烟碱和乙酰胆碱的轴突反射反应，尤其是在毛果芸香碱应用先于该过程时。烟碱样反应的抑制可能继发于M1拮抗作用，因为毛果芸香碱是M2激动剂和M1拮抗剂，而特异性M1拮抗剂哌仑西平产生了与毛果芸香碱类似的作用。
