Morgan T O, Delbridge L M
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
J Am Soc Nephrol. 1999 Jan;10 Suppl 11:S243-7.
Cardiac hypertrophy can be caused in different ways, and the effect of hypertrophy on prognosis depends on whether it is concentric or eccentric in nature. It is simplistic to ascribe hypertrophy purely to workload, and it is a complex interaction between workload, wall stress, and the local and humoral environment. In rats, acute elevation of BP occurring during the rats' sleep cycle causes cardiac hypertrophy, and reduction of BP in hypertensive rats during the sleep cycle causes reversal of left ventricular hypertrophy. This may be due to secretion of growth hormone and renin during sleep. Experimental evidence indicates that angiotensin II possibly formed and acting locally may be implicated in the genesis of cardiac hypertrophy; however, angiotensin II by itself causes relatively minor hypertrophy, but this becomes intensified if there is a high sodium intake and a high angiotensin II level. Blockade of the angiotensin system with angiotensin-converting enzyme inhibitors causes reversal of cardiac hypertrophy and similar results are achieved with AT1 receptor blocking drugs, suggesting that bradykinin may be of relatively minor importance. Clinically, the AT1 receptor blocking drugs have few side effects and appear to have similar beneficial effects to angiotensin-converting enzyme inhibitors, making them suitable to treat many people with hypertension.
心脏肥大可由多种方式引起，肥大对预后的影响取决于其本质上是同心性还是离心性。将肥大单纯归因于工作量是过于简单化的，它是工作量、壁应力以及局部和体液环境之间的复杂相互作用。在大鼠中，大鼠睡眠周期中出现的血压急性升高会导致心脏肥大，而睡眠周期中高血压大鼠的血压降低会导致左心室肥大的逆转。这可能是由于睡眠期间生长激素和肾素的分泌。实验证据表明，可能在局部形成并起作用的血管紧张素II可能与心脏肥大的发生有关；然而，血管紧张素II本身引起的肥大相对较小，但如果存在高钠摄入和高血管紧张素II水平，这种肥大就会加剧。用血管紧张素转换酶抑制剂阻断血管紧张素系统会导致心脏肥大的逆转，使用AT1受体阻断药物也能取得类似结果，这表明缓激肽可能相对不太重要。在临床上，AT1受体阻断药物副作用较少，似乎与血管紧张素转换酶抑制剂具有相似的有益效果，使其适合治疗许多高血压患者。
