Division of Pharmacology & Toxicology, Faculty of Pharmaceutical Sciences, University of British Columbia, 2146 East Mall, Vancouver, BC, V6T 1Z3, Canada.
Mol Cell Biochem. 2009 Dec;332(1-2):145-59. doi: 10.1007/s11010-009-0184-4. Epub 2009 Jun 18.
The metabolic syndrome is an important public health concern that predisposes individuals to the development of cardiovascular disease and/or Type 2 diabetes. The fructose-fed rat is an animal model of acquired systolic hypertension that displays numerous features of the metabolic syndrome. This animal model is used to study the relationship between insulin resistance/compensatory hyperinsulinemia and the development of hypertension. Several mechanisms have been proposed to mediate the link between insulin resistance and hypertension. In this review, we have addressed the role of sympathetic nervous system overactivation, increased production of vasoconstrictors, such as endothelin-1 and angiotensin II, and prostanoids in the development of hypertension in fructose-fed rats. The roles of nitric oxide, impaired endothelium-dependent relaxation and sex hormones in the pathogenesis of the fructose-fed induced hypertensive rats have also been highlighted. More recently, increased formation of reactive oxygen species and elevated levels of uric acid have been reported to contribute to fructose-induced hypertension.
代谢综合征是一个重要的公共健康关注点，它使个体易患心血管疾病和/或 2 型糖尿病。果糖喂养的大鼠是获得性收缩期高血压的动物模型，表现出许多代谢综合征的特征。这种动物模型用于研究胰岛素抵抗/代偿性高胰岛素血症与高血压发展之间的关系。已经提出了几种机制来介导胰岛素抵抗与高血压之间的联系。在这篇综述中，我们探讨了交感神经系统过度兴奋、内皮素-1 和血管紧张素 II 等血管收缩剂和前列腺素产生增加在果糖喂养大鼠高血压发展中的作用。还强调了一氧化氮、受损的内皮依赖性松弛和性激素在果糖喂养诱导的高血压大鼠发病机制中的作用。最近，据报道，活性氧的形成增加和尿酸水平升高有助于果糖诱导的高血压。
