Short-term incubation of equine laminar veins with cortisol and insulin alters contractility in vitro: possible implications for the pathogenesis of equine laminitis.
Authors: Keen, McGorum, Hillier, Nally
Journal: Journal of veterinary pharmacology and therapeutics
Summary
# Editorial Summary Cortisol and insulin exert complex and opposing effects on the contractility of small laminar veins, according to research by Keen and colleagues using isolated vessels from healthy horses and ponies studied via wire myography. When exposed to cortisol, laminar veins demonstrated heightened responsiveness to noradrenaline and serotonin (5-HT) but paradoxically reduced contractility to endothelin-1, whilst insulin exposure dampened vascular responses to phenylephrine and endothelin-1. These findings suggest a plausible vascular mechanism linking endocrine dysfunction to laminitis: excess cortisol could amplify venoconstrictor tone through enhanced catecholamine and serotonin sensitivity, whilst the blunted insulin response characteristic of insulin-resistant animals would compromise the hormone's protective counter-regulatory effect on alpha-adrenoreceptor and endothelin-mediated constriction. For practitioners managing horses with Cushing's disease or equine metabolic syndrome, these results provide mechanistic insight into why these animals face elevated laminitis risk, potentially supporting earlier intervention in cortisol or metabolic management as a preventative strategy alongside traditional farriery and nutritional approaches.
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Practical Takeaways
- •Horses with Cushing's disease or metabolic syndrome may have altered vascular reactivity in the laminae, increasing laminitis risk through cortisol-mediated changes in vein contraction
- •Insulin resistance may compound laminitis risk by reducing the natural protective effects of insulin on laminar blood vessel contraction
- •Management strategies targeting cortisol control and insulin sensitivity may help mitigate vascular mechanisms underlying laminitis in predisposed horses
Key Findings
- •Cortisol at 10⁻⁶ M significantly increased maximum contractility of laminar veins to noradrenaline and 5-hydroxytryptamine but decreased maximal contraction to endothelin-1
- •Insulin at 1000 μIU/mL decreased contractility of laminar veins to phenylephrine and endothelin-1
- •Short-term cortisol excess may enhance venoconstrictor responses in laminar veins in vivo, predisposing to laminitis
- •Reduced insulin counteraction of alpha-adrenoreceptor and endothelin-1-mediated contraction in insulin-resistant horses may exacerbate venoconstriction and laminitis risk