外泌汗腺

人体主要的汗腺

外泌汗腺(英語:eccrine sweat gland),又名小汗腺,是人体主要的汗腺[3],存在于几乎所有皮肤,尤以手掌和脚掌的密度为最高,头部次之,躯干及四肢较少,在其他哺乳动物中则较为稀疏,主要存在于无毛部位。人体发育过程中外泌汗腺密度最高可达200-400/cm²[4][5]

外泌汗腺
Gray940 - sweat gland.png
皮肤剖面图,黄色为外泌汗腺
细节
拉丁语Glandula sudorifera merocrina;
Glandula sudorifera eccrina
发育自外胚层[1]
系統外皮系统[1]
神经胆碱能交感神经[2]
识别标示
THH3.12.00.3.03009
FMAFMA:59154

外泌汗腺由顶端汗管、真皮导管和分泌小管组成。其中,顶端汗管(又名末端汗管)为一螺旋状导管;真皮导管为一外直内曲导管;分泌小管呈卷曲状,位于真皮或下皮英语hypodermis深处[6]

分泌编辑

外泌汗腺的分泌物是一种无菌的稀电解质溶液,主要成分有碳酸氢盐、钾和氯化钠(NaCl)[5],以及其他微量成分,如葡萄糖、丙酮酸、乳酸、细胞因子、免疫球蛋白、抗菌肽等[5]

汗液中Na+离子的浓度比血浆和细胞外液低得多(汗液约为40mM,血浆和细胞外液约为150mM)。外泌汗腺中的汗液最开始是含有高浓度Na+离子的,但Na+离子通过外泌汗腺导管细胞上的上皮钠通道英语epithelial sodium channels(ENaC)重吸收进入组织[7],减少了出汗过程中Na+的损失。ENaC突变亚基携带者会患有全身性假醛固酮减少症,Na+无法重吸收[8][9],分泌的汗液中Na+离子浓度会大大增加(高达180mmol/L)[8][10]

多汗症患者的汗腺(尤其是外泌汗腺)会对刺激做出过度反应,进而过度活跃,产生比一般人更多的汗液。囊腫性纖維化患者汗液中的Na+离子浓度也会增高。这两种病症是外泌汗腺导管细胞上的CFTR氯化物转运蛋白英语CFTR异常导致的[7]

参考资料编辑

  1. ^ 1.0 1.1 Neas, John F. Development of the Integumentary System. (编) Martini, Frederic H.; Timmons, Michael J.; Tallitsch, Bob. Embryology Atlas 4th. Benjamin Cumings. 
  2. ^ Krstic, Radivoj V. Human Microscopic Anatomy: An Atlas for Students of Medicine and Biology. Springer. 18 March 2004: 464. ISBN 9783540536666. 
  3. ^ our weird lack of hair may be the key to our success. 
  4. ^ James, William; Berger, Timothy; Elston, Dirk. Andrews' Diseases of the Skin: Clinical Dermatology 10th. Saunders. 2005: 6–7. ISBN 978-0-7216-2921-6. 
  5. ^ 5.0 5.1 5.2 Bolognia, J., Jorizzo, J., & Schaffer, J. (2012). Dermatology (3rd ed., pp. 539-544). [Philadelphia]: Elsevier Saunders.
  6. ^ Wilke, K.; Martin, A.; Terstegen, L.; Biel, S. S. A short history of sweat gland biology. International Journal of Cosmetic Science. June 2007, 29 (3): 169–179. ISSN 1468-2494. PMID 18489347. doi:10.1111/j.1467-2494.2007.00387.x. 
  7. ^ 7.0 7.1 Hanukoglu I, Boggula VR, Vaknine H, Sharma S, Kleyman T, Hanukoglu A. Expression of epithelial sodium channel (ENaC) and CFTR in the human epidermis and epidermal appendages. Histochemistry and Cell Biology. January 2017, 147 (6): 733–748. PMID 28130590. doi:10.1007/s00418-016-1535-3. 
  8. ^ 8.0 8.1 Hanukoglu A. Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects. The Journal of Clinical Endocrinology and Metabolism. Nov 1991, 73 (5): 936–44. PMID 1939532. doi:10.1210/jcem-73-5-936. 
  9. ^ Hanukoglu I, Hanukoglu A. Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases.. Gene. Jan 2016, 579 (2): 95–132. PMC 4756657. PMID 26772908. doi:10.1016/j.gene.2015.12.061. 
  10. ^ Edelheit, Oded; Hanukoglu, Israel; Shriki, Yafit; Tfilin, Matanel; Dascal, Nathan; Gillis, David; Hanukoglu, Aaron. Truncated beta epithelial sodium channel (ENaC) subunits responsible for multi-system pseudohypoaldosteronism (PHA) support partial activity of ENaC. The Journal of Steroid Biochemistry and Molecular Biology. 2010, 119 (1–2): 84–88. PMID 20064610. doi:10.1016/j.jsbmb.2010.01.002. 

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