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Journal of veterinary pharmacology and therapeutics2012; 36(4); 382-388; doi: 10.1111/j.1365-2885.2012.01429.x

Short-term incubation of equine laminar veins with cortisol and insulin alters contractility in vitro: possible implications for the pathogenesis of equine laminitis.

Abstract: This study investigated the effects of cortisol and insulin, hormones that affect both glycaemic status and vascular function, on the in vitro contractility of isolated healthy equine small laminar veins. Small veins (150-500 μm) draining the digital laminae from healthy horses or ponies were investigated by wire myography. Concentration response curves were constructed for noradrenaline (NA), phenylephrine (PE), endothelin-1 (ET-1) and 5-hydroxytryptamine (5-HT) in the presence of either cortisol (10(-6 ) m) or insulin (1000 μIU/mL). Cortisol significantly increased the maximum contractility of laminar veins to the vasoconstrictors NA and 5-HT but decreased the maximal contraction to ET-1. Insulin decreased the contractility of vessels to PE and ET-1. It is possible that short-term cortisol excess could enhance venoconstrictor responses to 5-HT and NA in laminar veins in vivo, thereby predisposing to laminitis. Additionally, a reduction in the ability of insulin to counteract alpha-adrenoreceptor and ET-1-mediated contraction, likely to occur in subjects with insulin resistance, may further exacerbate venoconstriction in animals prone to laminitis. These mechanisms may also predispose horses with disorders such as equine Cushing's disease and equine metabolic syndrome to laminitis.
Publication Date: 2012-09-03 PubMed ID: 22943152DOI: 10.1111/j.1365-2885.2012.01429.xGoogle Scholar: Lookup
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  • Journal Article

Summary

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The researchers conducted an experiment to study the impact of cortisol and insulin on the contractility of healthy small laminar veins in horses, and they suggest implications in the development of equine laminitis, a condition causing severe lameness and pain in horses.

Research Methods

  • The study involved the incubation of equine laminar veins (with a diameter ranging from 150-500 μm) with cortisol and insulin, hormones which are known to impact both blood sugar levels and vascular function.
  • The veins used in the experiments were extracted from healthy horses or ponies from the digital laminae. The veins’ behaviors were studied through wire myography.
  • Researches constructed concentration response curves for noradrenaline (NA), phenylephrine (PE), endothelin-1 (ET-1), and 5-hydroxytryptamine (5-HT) when these enzymes were present along with cortisol or insulin.

Key Findings

  • Cortisol notably increased the maximum contractility of laminar veins to the vasoconstrictors NA and 5-HT, implying a potential elevated risk for venoconstriction and, consequently, laminitis.
  • However, cortisol was found to decrease the highest contraction to ET-1, another vasoconstrictor.
  • Insulin, on the other hand, led to a decrease in contractility of veins in response to PE and ET-1.
  • The existence of insulin resistance, which reduces insulin’s ability to counteract alpha-adrenoreceptor and ET-1-mediated contraction, may compound the effect of venoconstriction, leading to a higher susceptibility to laminitis.

Implications

  • The results of the study suggest that animals experiencing short-term cortisol excess might be prone to an increased venoconstrictor response to 5-HT and NA, thereby predisposing these animals to laminitis.
  • The findings also indicate that disorders such as equine Cushing’s disease and equine metabolic syndrome, both of which can be associated with hormonal imbalances and insulin resistance, may lead to a heightened risk for laminitis in horses.

Cite This Article

APA
Keen JA, McGorum BC, Hillier C, Nally JE. (2012). Short-term incubation of equine laminar veins with cortisol and insulin alters contractility in vitro: possible implications for the pathogenesis of equine laminitis. J Vet Pharmacol Ther, 36(4), 382-388. https://doi.org/10.1111/j.1365-2885.2012.01429.x

Publication

ISSN: 1365-2885
NlmUniqueID: 7910920
Country: England
Language: English
Volume: 36
Issue: 4
Pages: 382-388

Researcher Affiliations

Keen, J A
  • Department of Biological and Biochemical Science, Glasgow Caledonian University, Glasgow, UK. John.Keen@ed.ac.uk
McGorum, B C
    Hillier, C
      Nally, J E

        MeSH Terms

        • Animals
        • Endothelin-1 / pharmacology
        • Hoof and Claw / blood supply
        • Hoof and Claw / pathology
        • Horse Diseases / etiology
        • Horse Diseases / metabolism
        • Horses
        • Hydrocortisone / pharmacology
        • Inflammation / etiology
        • Inflammation / metabolism
        • Inflammation / veterinary
        • Insulin / pharmacology
        • Norepinephrine / pharmacology
        • Phenylephrine / pharmacology
        • Serotonin / pharmacology
        • Vasoconstriction / drug effects
        • Veins / drug effects

        Citations

        This article has been cited 6 times.
        1. Pollard D, Wylie CE, Verheyen KLP, Newton JR. Identification of modifiable factors associated with owner-reported equine laminitis in Britain using a web-based cohort study approach.. BMC Vet Res 2019 Feb 12;15(1):59.
          doi: 10.1186/s12917-019-1798-8pubmed: 30755193google scholar: lookup
        2. Pakkanen SAE, de Vries A, Raekallio MR, Mykkänen AK, Palviainen MJ, Sankari SM, Vainio OM. Changes in energy metabolism, and levels of stress-related hormones and electrolytes in horses after intravenous administration of romifidine and the peripheral α-2 adrenoceptor antagonist vatinoxan.. Acta Vet Scand 2018 May 9;60(1):27.
          doi: 10.1186/s13028-018-0380-xpubmed: 29743097google scholar: lookup
        3. Nostell KE, Lindåse SS, Bröjer JT. Blood pressure in Warmblood horses before and during a euglycemic-hyperinsulinemic clamp.. Acta Vet Scand 2016 Oct 20;58(Suppl 1):65.
          doi: 10.1186/s13028-016-0247-ypubmed: 27766986google scholar: lookup
        4. Morgan RA, Keen JA, Walker BR, Hadoke PW. Vascular Dysfunction in Horses with Endocrinopathic Laminitis.. PLoS One 2016;11(9):e0163815.
          doi: 10.1371/journal.pone.0163815pubmed: 27684374google scholar: lookup
        5. Morgan R, Keen J, McGowan C. Equine metabolic syndrome.. Vet Rec 2015 Aug 15;177(7):173-9.
          doi: 10.1136/vr.103226pubmed: 26273009google scholar: lookup
        6. Menzies-Gow NJ, Wray H, Bailey SR, Harris PA, Elliott J. The effect of tumour necrosis factor-α and insulin on equine digital blood vessel function in vitro.. Inflamm Res 2014 Aug;63(8):637-47.
          doi: 10.1007/s00011-014-0736-2pubmed: 24764104google scholar: lookup