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

被引:11
|
作者
Keen, J. A. [1 ,2 ]
McGorum, B. C. [2 ]
Hillier, C. [1 ,3 ]
Nally, J. E. [1 ]
机构
[1] Glasgow Caledonian Univ, Dept Biol & Biochem Sci, Glasgow G4 0BA, Lanark, Scotland
[2] Univ Edinburgh, Easter Bush Vet Ctr, RDSVS, Roslin, Midlothian, Scotland
[3] Univ W Indies, Bridgetown, Barbados
关键词
STANDARD-BRED HORSES; CLINICALLY NORMAL PONIES; DIGITAL STARLING FORCES; CUSHINGS-SYNDROME; VASCULAR-RESPONSES; GLUCOSE-TOLERANCE; NITRIC-OXIDE; RISK-FACTORS; ENDOTHELIN-1; RESISTANCE;
D O I
10.1111/j.1365-2885.2012.01429.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 (150-500m) 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 (1000IU/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.
引用
收藏
页码:382 / 388
页数:7
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