کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2894998 1172447 2006 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Aortic thromboxane receptor deficiency alters vascular reactivity in cholesterol-fed rabbits
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Aortic thromboxane receptor deficiency alters vascular reactivity in cholesterol-fed rabbits
چکیده انگلیسی
Hypercholesterolemia is considered a major risk factor in the development of atherosclerotic disease. The endothelium is the source of a number of vasoactive compounds which may be altered by the disease process. For example, synthesis of the arachidonic acid metabolite thromboxane A2 (TXA2) increases in atherosclerosis. Non-selective blockade of vascular and platelet thromboxane (TP) receptors retards the progression of the disease in various animal models. We have previously identified a subset of NZW rabbits that lack only vascular (v) TP receptors, referred to as vTP−. These rabbits provide a unique model to elucidate the role of vascular TP receptors in hypercholesterolemia. Studies evaluated vascular responses to phenylephrine and acetylcholine in isolated aortic rings obtained from vTP− and vTP+ rabbits fed 0.5% cholesterol diet for a period of only 3 weeks. In the cholesterol-fed vTP− rabbits, contractions to phenylephrine were reduced compared to the vTP+ cholesterol-fed rabbits. Acetylcholine-induced relaxations were greater in cholesterol-fed vTP− rabbits compared to cholesterol-fed vTP+ rabbits. While the overall incidence of aortic lesions was small after only 3 weeks of cholesterol-feeding, results indicated a reduction in lesions in the vTP− compared to the vTP+ rabbits. In summary, these studies are the first to show that if rabbits lack only vascular TP receptors, impaired vascular reactivity responses normally associated with hypercholesterolemia are diminished.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Atherosclerosis - Volume 189, Issue 2, December 2006, Pages 358-363
نویسندگان
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