Lindpaintner K, Sen S
Circ Res. 1985 Oct;57(4):610-7. doi: 10.1161/01.res.57.4.610.
Cardiac hypertrophy in systemic hypertension may not result simply from increased afterload. Previous studies indicate that factors other than blood pressure may influence cardiac hypertrophy. We evaluated the effects of dietary sodium restriction in two-kidney one-clip renal hypertensive rats. After the renal artery had been clipped, the rats received a normal diet until hypertension was established; thereafter, a sodium-deficient diet was instituted in one group. Clipped rats on a regular diet had significantly higher systolic blood pressures than sham-operated controls (205 +/- 9 vs. 129 +/- 1 mm Hg, respectively). Sodium restriction did not reverse hypertension (190 +/- 8 mm Hg), but led to a significant reduction of relative heart weight compared to rats on the normal diet (2.94 +/- 0.24 vs. 3.86 +/- 0.23 mg/g, respectively; P less than 0.01). The hypertrophied hearts of animals on the regular diet showed depressed tissue catecholamines (significant only for norepinephrine); sodium restriction resulted in a restoration to normal levels. Thus, we demonstrated a dissociation of blood pressure and cardiac hypertrophy in the two-kidney one-clip model, similar to previous findings in other models. Our results support the concept that factors other than blood pressure contribute to cardiac hypertrophy. Dietary sodium intake appears to be one such factor. In addition, a possible role of the sympathetic nervous system is suggested.
系统性高血压中的心脏肥大可能并非仅仅由后负荷增加所致。先前的研究表明,血压以外的因素可能影响心脏肥大。我们评估了在二肾一夹肾性高血压大鼠中限制饮食钠摄入的作用。肾动脉夹闭后,大鼠接受正常饮食直至高血压形成;此后,一组大鼠开始摄入缺钠饮食。常规饮食的夹闭大鼠收缩压显著高于假手术对照组(分别为205±9与129±1毫米汞柱)。钠限制并未逆转高血压(190±8毫米汞柱),但与正常饮食的大鼠相比,导致相对心脏重量显著降低(分别为2.94±0.24与3.86±0.23毫克/克;P<0.01)。常规饮食动物的肥大心脏显示组织儿茶酚胺水平降低(仅去甲肾上腺素显著);钠限制导致其恢复至正常水平。因此,我们在二肾一夹模型中证明了血压与心脏肥大的分离,类似于先前在其他模型中的发现。我们的结果支持这样一种观点,即血压以外的因素促成了心脏肥大。饮食钠摄入似乎就是这样一个因素。此外,提示了交感神经系统可能发挥的作用。