The tissue renin-angiotensin system in rats with fructose-induced hypertension: overexpression of type 1 angiotensin II receptor in adipose tissue
The tissue renin-angiotensin system in rats with fructose-induced hypertension: overexpression of type 1 angiotensin II receptor in adipose tissue
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DOI：
10.1097/00004872-200018060-00006
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发表时间：
2000-06-01
影响因子：
4.9
通讯作者：
Schambelan, M
中科院分区：
文献类型：
--
作者：
Giacchetti, G;Sechi, LA;Schambelan, M
目的果糖喂养诱导SD大鼠高血压、胰岛素抵抗和高血脂。果糖引起的高血压的机制尚不清楚。在此，我们研究了果糖喂养和不同盐摄入量对高血压模型中血压、葡萄糖耐量、血浆肾素活性和组织血管紧张素原、肾素和AT（1）受体mRNA水平的影响。用标准大鼠饲料或含66%果糖的饲料喂养Sprague-Dawley大鼠，测定大鼠组织中的肾素和血管紧张素II 1型（AT（1））受体mRNA水平。果糖组大鼠血清甘油三酯（P < 0.05）和甘油三酯（P < 0.01）水平显著高于对照组。果糖喂养组大鼠的血糖和胰岛素对口服葡萄糖负荷的反应显著高于对照组（P < 0.05）。在果糖喂养的动物和对照动物之间，肝脏和脂肪中的血管紧张素原mRNA水平以及肾脏中的肾素mRNA水平没有差异。果糖组大鼠脂肪中AT（1）受体mRNA水平显著高于对照组（P < 0.05），但肾脏中AT（1）受体mRNA水平则无显著差异。为了确定果糖诱导的高血压是否依赖于饮食中的盐含量，给大鼠喂食标准大鼠饲料和富含果糖的饮食，其中含有低和高浓度的氯化钠。高盐饮食组血压显著升高（P < 0.05）。结论果糖可诱导正常或高盐饮食动物的高血压，且与脂肪组织AT（1）受体表达增加有关。这些发现表明AT（1）受体可能在果糖喂养引起的代谢和血流动力学异常的病理生理学中起作用。J Hypertens 2000，18：695-702（C）Lippincott威廉姆斯& Wilkins.
Objective Fructose feeding induces hypertension, insulin-resistance and hypertriglyceridemia in Sprague-Dawley rats. The mechanisms of fructose-induced hypertension are as yet unknown. Here we investigate the effects of fructose feeding and of varying salt intake on blood pressure, glucose tolerance, plasma renin activity, and tissue angiotensinogen, renin, and AT(1) receptor mRNA levels in this model of hypertension.Design and methods To investigate the role of the renin-angiotensin system in fructose-induced hypertension we measured angiotensinogen, renin and angiotensin II type 1 (AT(1)) receptor mRNA levels in tissues of Sprague-Dawley rats that were fed either standard rat chow or a diet containing 66% fructose.Results Blood pressure (P < 0.05) and triglyceride (P < 0.01) levels were significantly greater in the fructose-fed animals. Plasma glucose and insulin responses to an oral glucose load were significantly greater (P < 0.05) in fructose-fed than control rats. Angiotensinogen mRNA levels in liver and fat, and renin mRNA levels in kidney did not differ between fructose-fed and control animals. Levels of AT(1) receptor mRNA were significantly greater in the fat obtained from fructose-fed rats than in that from control rats (P < 0.05), but this was not so in the kidney. To determine whether fructose-induced hypertension is dependent on dietary salt content, rats were fed standard rat chow and a fructose-enriched diet with low and high sodium chloride concentrations. Blood pressure increased significantly (P < 0.05) only in the fructose-fed rats receiving the high-salt diet. Similarly, increased AT(1) receptor mRNA levels were observed only in the fructose-fed rats that were maintained on the high-salt dietConclusions Fructose feeding induces hypertension in normal- or high-salt fed animals and it is associated with an increased expression of the AT(1) receptor in adipose tissue. These findings suggest that AT(1) receptors might play a role in the pathophysiology of metabolic and hemodynamic abnormalities induced by fructose feeding. J Hypertens 2000, 18:695-702 (C) Lippincott Williams & Wilkins.