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Eccrine sweat gland

From Wikipedia, the free encyclopedia
Eccrine sweat gland
A sectional view of the skin (magnified), with eccrine glands highlighted.
NerveCholinergic sympathetic nerves[2]
Latinglandula sudorifera merocrina;
glandula sudorifera eccrina
Anatomical terminology

Eccrine sweat glands (/ˈɛkrən, -ˌkrn, -ˌkrn/; from Greek ek(s)+krinein 'out(wards)/external+secrete')[3] are the major sweat glands of the human body.[4] Eccrine sweat glands are found in virtually all skin, with the highest density in the palms of the hands, and soles of the feet, and on the head, but much less on the torso and the extremities. In other mammals, they are relatively sparse, being found mainly on hairless areas such as foot pads. They reach their peak of development in humans, where they may number 200–400/cm2 of skin surface.[5][6] They produce sweat, a merocrine secretion which is clear, odorless substance, consisting primarily of water. These are present from birth. Their secretory part is present deep inside the dermis.

Eccrine glands are composed of an intraepidermal spiral duct, the "acrosyringium"; a dermal duct, consisting of a straight and coiled portion; and a secretory tubule, coiled deep in the dermis or hypodermis.[7] The eccrine gland opens out through the sweat pore. The coiled portion is formed by two concentric layers of columnar or cuboidal epithelial cells.[8] The epithelial cells are interposed by the myoepithelial cells. Myoepithelial cells support the secretory epithelial cells. The duct of eccrine gland is formed by two layers of cuboidal epithelial cells.[9]

Eccrine glands are active in thermoregulation by providing cooling from water evaporation of sweat secreted by the glands on the body surface and emotionally induced sweating (anxiety, fear, stress, and pain).[6][7] The white sediment in otherwise colorless eccrine secretions is caused by evaporation that increases the concentration of salts.

The odor from sweat is due to bacterial activity on the secretions of the apocrine sweat glands, a distinctly different type of sweat gland found in human skin.

Eccrine glands are innervated only by the sympathetic nervous system. Postganglionic sympathetic fibers innervating the cutaneous district can produce either noradrenaline or acetylcholine as neurotransmitters depending on the target structure.[10] The sympathetic cholinergic fibers connecting with the sweat glands discharge primarily by changes in deep body temperature (core temperature).[11] The glands on palms and soles do not respond only to temperature stimuli but secrete at times of emotional stress.


The secretion of eccrine glands is a sterile, dilute electrolyte solution with primary components of bicarbonate, potassium, and sodium chloride (NaCl),[6] and other minor components that may include glucose, pyruvate, lactate, cytokines, immunoglobulins, antimicrobial peptides such as dermcidin, and many others.[6][12]

Relative to the plasma and extracellular fluid, the concentration of Na+ ions is much lower in sweat (~40 mM in sweat versus ~140 mM in plasma and extracellular fluid). Initially, within the eccrine glands, sweat has a high concentration of Na+ ions. The Na+ ions are re-absorbed into the tissue via the epithelial sodium channels (ENaCs) that are located on the apical membrane of the cells that form the eccrine gland ducts (see Fig. 9 and Fig. 10 of the reference).[9] This re-uptake of Na+ ions reduces the loss of Na+ during the process of perspiration. People with the systemic pseudohypoaldosteronism syndrome who carry mutations in the ENaC subunit genes have salty sweat as they cannot reabsorb the salt in sweat.[13][14] Sometimes these Na+ ion concentrations can greatly increase (up to 180 mmol/L).[13] [15]

In people who have hyperhidrosis, the sweat glands (eccrine glands in particular) overreact to stimuli and are just generally overactive, producing more sweat than normal. Similarly, people with cystic fibrosis also produce salty sweat. But in these cases, the problem is in the CFTR chloride transporter that is also located on the apical membrane of eccrine gland ducts.[9]

See also[edit]

List of distinct cell types in the adult human body


  1. ^ a b Neas, John F. "Development of the Integumentary System". In Martini, Frederic H.; Timmons, Michael J.; Tallitsch, Bob (eds.). Embryology Atlas (4th ed.). Benjamin Cumings. Archived from the original on 2012-08-08. Retrieved 2012-12-21.
  2. ^ Krstic, Radivoj V. (18 March 2004). Human Microscopic Anatomy: An Atlas for Students of Medicine and Biology. Springer. p. 464. ISBN 9783540536666.
  3. ^ McKean, Erin (2005). "eccrine". The New Oxford American Dictionary (2 ed.). ISBN 9780195170771.
  4. ^ "our weird lack of hair may be the key to our success".
  5. ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. pp. 6–7. ISBN 978-0-7216-2921-6.
  6. ^ a b c d Bolognia, J., Jorizzo, J., & Schaffer, J. (2012). Dermatology (3rd ed., pp. 539-544). [Philadelphia]: Elsevier Saunders.
  7. ^ a b Wilke, K.; Martin, A.; Terstegen, L.; Biel, S. S. (June 2007). "A short history of sweat gland biology". International Journal of Cosmetic Science. 29 (3): 169–179. doi:10.1111/j.1467-2494.2007.00387.x. ISSN 1468-2494. PMID 18489347. S2CID 205556581.
  8. ^ Cui, Chang-Yi; Schlessinger, David (2015). "Eccrine sweat gland development and sweat secretion". Experimental Dermatology. 24 (9): 644–650. doi:10.1111/exd.12773. ISSN 0906-6705. PMC 5508982. PMID 26014472.
  9. ^ a b c Hanukoglu I, Boggula VR, Vaknine H, Sharma S, Kleyman T, Hanukoglu A (January 2017). "Expression of epithelial sodium channel (ENaC) and CFTR in the human epidermis and epidermal appendages". Histochemistry and Cell Biology. 147 (6): 733–748. doi:10.1007/s00418-016-1535-3. PMID 28130590. S2CID 8504408.
  10. ^ Donadio, V., Incensi, A., Vacchiano, V. et al. The autonomic innervation of hairy skin in humans: an in vivo confocal study. Sci Rep 9, 16982 (2019). https://doi.org/10.1038/s41598-019-53684-3
  11. ^ Neural control of sweat secretion: a review* Y. Hu, C. Converse, M.C. Lyons and W.H. Hsu iD Department of Biomedical Sciences, Iowa State University, 1800 S. 16th Street, Ames, IA 50011-1250, U.S.A. Linked Comment: Morris-Jones. Br J Dermatol 2018; 178:1233–1234
  12. ^ Niyonsaba, F; Suzuki, A; Ushio, H; Nagaoka, I; Ogawa, H; Okumura, K (2009). "The human antimicrobial peptide dermcidin activates normal human keratinocytes". The British Journal of Dermatology. 160 (2): 243–9. doi:10.1111/j.1365-2133.2008.08925.x. PMID 19014393. S2CID 26601547.
  13. ^ a b Hanukoglu A (Nov 1991). "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. 73 (5): 936–44. doi:10.1210/jcem-73-5-936. PMID 1939532.
  14. ^ Hanukoglu I, Hanukoglu A (Jan 2016). "Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases". Gene. 579 (2): 95–132. doi:10.1016/j.gene.2015.12.061. PMC 4756657. PMID 26772908.
  15. ^ Edelheit, Oded; Hanukoglu, Israel; Shriki, Yafit; Tfilin, Matanel; Dascal, Nathan; Gillis, David; Hanukoglu, Aaron (2010). "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. 119 (1–2): 84–88. doi:10.1016/j.jsbmb.2010.01.002. PMID 20064610. S2CID 9564777.

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