RELATIONSHIP BETWEEN DIETARY-SODIUM INTAKE, HEMODYNAMICS, AND CARDIAC MASS IN SHR AND WKY RATS
RELATIONSHIP BETWEEN DIETARY-SODIUM INTAKE, HEMODYNAMICS, AND CARDIAC MASS IN SHR AND WKY RATS
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DOI：
10.1152/ajpregu.1993.264.1.r30
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发表时间：
1993-01-01
影响因子：
--
通讯作者：
PEGRAM, BL
中科院分区：
文献类型：
--
作者：
FROHLICH, ED;CHIEN, YW;PEGRAM, BL
为了研究钠摄入量对循环稳态和心脏结构的影响，测定了自发性高血压(SHR)和正常血压Wistar-京都(WKY)大鼠控制摄入低钠(0.01%)、标准钠(0.44%)和高钠(1.44%和4%)10周后心脏质量、全身血流动力学和器官血流量的变化。采用放射性微球参照法测定清醒大鼠的全身和局部血流动力学。不同的饮食钠操作没有引起WKY大鼠全身和局部血流动力学的任何变化。相反，高钠饮食使SHR大鼠的动脉压和总外周阻力逐渐增加，而心脏指数、心率和流向心脏、肾脏和内脏的器官血液减少。较高的钠摄入量(4%)增加了SHR和WKY大鼠的总质量指数和左心室重量指数，尽管WKY大鼠的血流动力学没有变化。这些数据表明，高钠饮食除了引起全身血管收缩和高血压加重外，还进一步增加了SHR大鼠的心脏质量；它还增加了WKY大鼠的心脏质量，而不依赖于动脉压的变化，提示高钠摄入可能是心肌肥厚发展的一个独立的致病因素。
To study the effects of sodium intake on circulatory homeostasis and cardiac structure, changes in cardiac mass, systemic hemodynamics, and organ blood flows were determined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats after 10 wk of controlled dietary intake of low sodium (0.01%), standard sodium (0.44%), and high sodium (2 levels: 1.44 and 4%). Systemic and regional hemodynamics were measured in conscious rats using the radioactive microsphere reference method. The various dietary sodium manipulations did not cause any changes in systemic and regional hemodynamics in the WKY rats. In contrast, the high-sodium diets increased arterial pressure and total peripheral resistance progressively in the SHR rats while decreasing cardiac index, heart rate, and organ blood flows to heart, kidneys, and splanchnic ama. The higher sodium intake (4%) increased total and left ventricular mass index in both the SHR and the WKY rats even though hemodynamics of the WKY rats remained unchanged. These data indicate that the high-sodium diet, in addition to producing general vasoconstriction and exacerbation of hypertension, increased cardiac mass further in SHR rats; it also increased cardiac mass in the WKY rats independent of arterial pressure changes, suggesting that high sodium intake may be an independent pathogenetic factor for the development of cardiac hypertrophy.