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

Authors

  • J. A. Keen,

    Corresponding author
    1. Royal (Dick) School of Veterinary Studies (R(D)SVS), The University of Edinburgh, Easter Bush Veterinary Centre, Roslin, Midlothian, UK
    • Department of Biological and Biochemical Science, Glasgow Caledonian University, Glasgow, UK
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  • B. C. McGorum,

    1. Royal (Dick) School of Veterinary Studies (R(D)SVS), The University of Edinburgh, Easter Bush Veterinary Centre, Roslin, Midlothian, UK
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  • C. Hillier,

    1. Department of Biological and Biochemical Science, Glasgow Caledonian University, Glasgow, UK
    2. University of the West Indies, Cave Hill Campus, Barbados, West Indies
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  • J. E. Nally

    1. Department of Biological and Biochemical Science, Glasgow Caledonian University, Glasgow, UK
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John Keen, Easter Bush Veterinary Centre, Roslin, Midlothian EH25 9RG, UK. E-mail: John.Keen@ed.ac.uk

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.

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