Dietary-sodium-induced cardiac remodeling in spontaneously hypertensive rat versus Wistar-Kyoto rat
Dietary-sodium-induced cardiac remodeling in spontaneously hypertensive rat versus Wistar-Kyoto rat
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DOI：
10.1097/00004872-199816060-00020
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发表时间：
1998-06-01
影响因子：
4.9
通讯作者：
Yuan, BX
中科院分区：
文献类型：
--
作者：
Leenen, FHH;Yuan, BX
Objective.研究短期和长期高钠摄入对钠敏感性自发性高血压大鼠和钠抵抗性Wistar-Kyoto大鼠心脏质量和结构的影响。将年轻的自发性高血压大鼠和Wistar-Kyoto大鼠随机分配到对照饮食、2%或8%的饮食钠2-12周，并评价静息血流动力学、心脏血管紧张素II水平、交感神经活性和心脏结构的变化。交感神经活性通过测量血浆儿茶酚胺水平、血压对神经节阻滞的反应和去甲肾上腺素的心脏周转率来评估。高钠摄入4周增加了4周龄的Wistar-Kyoto大鼠的左心室重量（2和8%NaCl饮食分别增加了11%和25%）。然而，这种肥大反应是暂时的，在6周后已经减弱，并且在高钠摄入12周后消失。然而，在长时间暴露后，发生了向心性重塑（即左心室壁厚：半径比增加，而左心室质量无变化）。高钠摄入量不影响静息血压，心脏指数，心脏血管紧张素II水平，和一般的交感神经活性的Wistar-Kyoto大鼠。短期高钠摄入量不会增加年轻自发性高血压大鼠的左心室质量，除非钠摄入量太高（8%NaCl），血压和一般交感神经活动也增加。然而，长期适度（2%）增加钠摄入量也会引起自发性高血压大鼠的向心性重构，而不会增加左心室质量、血压、心脏指数以及全身和心脏交感神经活动。年轻的Wistar-Kyoto大鼠的血压是钠不敏感的，但心脏结构是钠敏感的，高膳食钠摄入导致早期肥大反应，然后向心性重塑。相反，在自发性高血压大鼠中，肥厚反应似乎发生在血压反应之后，而重构与Wistar-Kyoto大鼠相似。(C)1998 Lippincott-Raven出版社。
Objective. To study the effects of short-term and longterm high sodium intake on cardiac mass and design in sodium-sensitive spontaneously hypertensive rats versus sodium-resistant Wistar-Kyoto rats.Methods. Young spontaneously hypertensive rats and Wistar-Kyoto rats were randomly allocated to control diet, 2 or 8% dietary sodium for 2-12 weeks and changes in resting hemodynamics, cardiac angiotensin II level, sympathetic activity and cardiac structure evaluated. Sympathetic activity was assessed by measuring levels of plasma catecholamines, responses of blood pressure to ganglionic blockade, and rates of cardiac turnover of norepinephrine.Results. High sodium intake for 4 weeks increased left ventricle weight of Wistar-Kyoto rats aged 4 weeks (by 11 and 25% for 2 and 8% NaCl diets, respectively). This hypertrophic response was temporary, however, had already diminished after 6 weeks, and was absent after 12 weeks of a high sodium intake. However, after prolonged exposure concentric remodeling occurred (i.e. left ventricle wall thickness:radius ratio increased with no change in left ventricle mass). High sodium intake did not affect resting blood pressure, cardiac index, cardiac angiotensin II level, and general sympathetic activity of Wistar-Kyoto rats. Short-term high sodium intake did not increase left ventricle mass of young spontaneously hypertensive rats, unless sodium intake was so high (8% NaCl) that blood pressure and general sympathetic activity increased, too. However, a prolonged moderate (2%) increase in sodium intake also caused concentric remodeling in spontaneously hypertensive rats without increasing left ventricle mass, blood pressure, cardiac index, and general and cardiac sympathetic activities.Conclusions. The blood pressure in young Wistar-Kyoto rats is sodium-insensitive but the heart structure is sodium-sensitive and high dietary sodium intake causes an early hypertrophic response, and then concentric remodeling. In contrast, hypertrophic response appears to occur after the response of blood pressure in spontaneously hypertensive rats, whereas the remodeling is similar to that in Wistar-Kyoto rats. (C) 1998 Lippincott-Raven Publishers.