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Veterinary dermatology2007; 18(3); 152-160; doi: 10.1111/j.1365-3164.2007.00585.x

A preliminary study of the short circuit current (Isc) responses of sweat gland cells from normal and anhidrotic horses to purinergic and adrenergic agonists.

Abstract: The causal factors of equine anhidrosis have not yet been elucidated but defective electrolyte transport mechanisms in the gland are likely to be involved. To investigate this possibility, experiments were performed on cultured equine sweat gland epithelia from five free-sweating UK horses (3 intact males, 2 mares, aged 2-4 years) and from three free-sweating Singapore horses (1 intact male, 2 mares, aged 3-5 years) and three anhidrotic (Singapore) horses (1 intact male, 1 gelding, 1 mare, aged 3-6 years). Cultured cells from each animal were grown on permeable supports and loaded into Ussing chambers to quantify transepithelial resistance and agonist-induced electrolyte transport by the short circuit current (Isc) technique. Transepithelial resistances across the layers of cultured cells were not significantly different between cells from UK and Singapore free-sweating horses, but were significantly reduced in anhidrotic animals. Purinergic agonists added to the apical and basolateral aspects of the cultured cells caused similar increases in Isc between the two populations of unaffected cells, but Isc increases were significantly reduced in anhidrotic animals. Beta-adrenergic agonist stimulation of the anhidrotic cell layers failed to elicit any change in Isc. These pilot results not only confirm earlier conclusions from anatomical findings that failure in the secretory process occurs in anhidrosis but also indicate that both of the known ion transport mechanisms are involved. The trigger for these failures warrants further investigation.
Publication Date: 2007-05-02 PubMed ID: 17470229DOI: 10.1111/j.1365-3164.2007.00585.xGoogle Scholar: Lookup
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  • Journal Article

Summary

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The research investigates the underlying causes of anhidrosis (inability to sweat) in horses, suggesting that faulty electrolyte transport in sweat glands could be a contributing factor. Evidence came from experiments with sweat gland cells cultured from horses, with results signaling significant differences between cells from regular sweating (free-sweating) and anhidrotic horses.

Experimental Design and Samples

  • The researchers collected sweat gland epithelial samples from five UK and eight Singapore horses, which included both normal, free-sweating horses and anhidrotic horses.
  • These included female (mares) and male (intact males and geldings) horses ageing 2 to 6 years, providing variety in gender and age.
  • The cultured cells from each animal were set on permeable supports for a more controlled environment and quantitative measurements.

Methodology for Evaluation

  • Cells were placed in Ussing chambers to calculate their transepithelial resistance and measure the electrolyte transport through the short circuit current (Isc) technique.
  • The transepithelial resistance is vital because it determines the amount of electrical resistance across a cell barrier, which indirectly reflects ions’ transport through cells.
  • The changes in the short circuit current give insight into the functioning electrolyte transport mechanisms of the sweat gland cells.

Key Findings

  • All the free-sweating horses from both UK and Singapore displayed no significant difference in transepithelial resistances across the cultured cells.
  • However, the cells from anhidrotic horses showed significantly lower transepithelial resistance, indicating impaired electrolyte transport operations.
  • When the researchers added purinergic agonists to the cultured cells, the unaffected cells displayed similar increases in Isc. By contrast, the Isc boost in anhidrotic animals was notably less.
  • The use of beta-adrenergic agonist to stimulate anhidrotic cells resulted in no change in Isc, confirming the cells’ non-responsive state.

Implications and Recommendations

  • The results of this study not only affirm the current understanding of anhidrosis in horses, connecting issues in the sweat glands’ secretory processes, but also suggest a defect in both known ion transport mechanisms.
  • The reason behind these defects, which might act as the potential trigger for anhidrosis, is left open for further investigation.

Cite This Article

APA
Wilson DC, Corbett AD, Steel C, Pannirselvam R, Bovell DL. (2007). A preliminary study of the short circuit current (Isc) responses of sweat gland cells from normal and anhidrotic horses to purinergic and adrenergic agonists. Vet Dermatol, 18(3), 152-160. https://doi.org/10.1111/j.1365-3164.2007.00585.x

Publication

ISSN: 0959-4493
NlmUniqueID: 9426187
Country: England
Language: English
Volume: 18
Issue: 3
Pages: 152-160

Researcher Affiliations

Wilson, Darius C S
  • School of Life Sciences, Glasgow Caledonian University, Glasgow, UK.
Corbett, Alistair D
    Steel, Cate
      Pannirselvam, Roshni
        Bovell, Douglas L

          MeSH Terms

          • Adrenergic Agonists / pharmacology
          • Animals
          • Cells, Cultured
          • Dose-Response Relationship, Drug
          • Electrophysiology
          • Epithelial Cells / metabolism
          • Extracellular Space / metabolism
          • Female
          • Horse Diseases / physiopathology
          • Horses / physiology
          • Hypohidrosis / physiopathology
          • Hypohidrosis / veterinary
          • Ion Channels / drug effects
          • Ion Channels / metabolism
          • Ion Transport / drug effects
          • Isoproterenol / pharmacology
          • Male
          • Purines / pharmacology
          • Receptors, Purinergic / metabolism
          • Sweat Glands / cytology
          • Sweat Glands / drug effects
          • Sweating / drug effects

          Citations

          This article has been cited 1 times.
          1. Patterson Rosa L, Mallicote MF, MacKay RJ, Brooks SA. Ion Channel and Ubiquitin Differential Expression during Erythromycin-Induced Anhidrosis in Foals.. Animals (Basel) 2021 Nov 25;11(12).
            doi: 10.3390/ani11123379pubmed: 34944156google scholar: lookup