Sen S, Tarazi R C
J Hypertens Suppl. 1986 Oct;4(3):S123-6.
In 1974 we reported that left ventricular mass correlated poorly with blood pressure levels during both the development and the reversal of hypertensive cardiac hypertrophy. This study, which was confirmed by many, has since been extended along two main lines: investigation of the factors modulating left ventricular hypertrophy and of associated changes in contractile protein, and comparison of the left ventricular structural response to hypertension with those of the large and small resistance vessels. In addition to blood pressure control, two factors were identified as important modulators of left ventricular hypertrophy: the level of cardioadrenergic activity and a recently isolated myocardial factor in SHR which stimulates in vitro cardiac protein synthesis. Of greater importance haemodynamically are the structural changes in the small resistance vessels; these were estimated from resistance to constant flow during maximal vasodilatation (Folkow). Captopril-hydrochlorothiazide led to a significantly greater reduction in that index than hydralazine, although both led to equal blood pressure control. Despite some general parallelism, the structural cardiovascular responses to hypertension were not homogeneous; important differences were found among the heart, aorta and resistance vessels. The development and regression of cardiovascular hypertrophy are not dependent on mechanical load alone but seem to be modulated at three levels - increased pressure load, level of cardioadrenergic activity and local growth factor.
1974年我们报告称，在高血压性心肌肥厚的发展和逆转过程中，左心室质量与血压水平的相关性较差。这项得到许多人证实的研究此后沿着两条主线进行了扩展：对调节左心室肥厚的因素以及收缩蛋白相关变化的研究，以及将左心室对高血压的结构反应与大小阻力血管的反应进行比较。除了血压控制外，还确定了两个作为左心室肥厚重要调节因子的因素：心脏肾上腺素能活性水平和最近在自发性高血压大鼠中分离出的一种刺激体外心脏蛋白质合成的心肌因子。从血流动力学角度来看，更重要的是小阻力血管的结构变化；这些变化是根据最大血管舒张时对恒定血流的阻力来估算的（福尔科）。尽管卡托普利 - 氢氯噻嗪和肼屈嗪都能使血压得到同等控制，但前者导致该指标的降低幅度明显大于后者。尽管存在一些总体上的相似性，但心血管系统对高血压的结构反应并不一致；在心脏、主动脉和阻力血管之间发现了重要差异。心血管肥厚的发展和消退并非仅取决于机械负荷，而是似乎在三个层面受到调节——压力负荷增加、心脏肾上腺素能活性水平和局部生长因子。
