Devereux R B, Pickering T G, Cody R J, Laragh J H
J Clin Hypertens. 1987 Mar;3(1):87-103.
This article examines available data concerning the hypothesis that the renin-angiotensin system directly stimulates cardiac hypertrophy and dysfunction in hypertension. Several experiments support a direct effect of angiotensin on myocardial protein synthesis and suggest that this may be independent of adrenergic influences. However, the role played by the renin system in the pathogenesis of hypertensive cardiac hypertrophy may be small, for left ventricular (LV) muscle mass is not systematically greater in high-renin as opposed to low-renin forms of experimental or human hypertension. In animal studies, regression of LV hypertrophy is more consistently observed in response to drugs that inhibit as opposed to those that stimulate renin-angiotensin system activity (i.e., converting enzyme inhibitors or beta-adrenoceptor blockers vs. diuretics or direct vasodilators), although the difference is more quantitative than absolute. Similarly, significant reductions in LV mass occurred in 13 of 16 human trials with converting enzyme inhibitors or beta blockers as opposed to 2 of 10 trials with diuretics or vasodilators (mean = 7.11; p less than 0.01). However, uncertainties regarding the degree of reduction in angiotensin II and adrenergic effects, possible interactions between these systems, and incomplete characterization of induced changes in hemodynamic load on the heart all limit the interpretation of available studies. Preliminary data suggest that an inverse relation exists between renin-angiotensin system activity and LV systolic performance in primary and secondary human hypertension, a possibility that merits further study.
本文研究了有关肾素 - 血管紧张素系统直接刺激高血压患者心脏肥大和功能障碍这一假说的现有数据。多项实验支持血管紧张素对心肌蛋白合成有直接作用，并表明这可能独立于肾上腺素能影响。然而，肾素系统在高血压性心脏肥大发病机制中所起的作用可能较小，因为在实验性或人类高血压的高肾素型与低肾素型中，左心室（LV）肌肉质量并非系统性地更高。在动物研究中，与刺激肾素 - 血管紧张素系统活性的药物（即利尿剂或直接血管扩张剂）相比，使用抑制该系统活性的药物（即转换酶抑制剂或β - 肾上腺素能受体阻滞剂）时，更一致地观察到左心室肥大的消退，尽管这种差异更多是数量上的而非绝对的。同样，在16项使用转换酶抑制剂或β受体阻滞剂的人体试验中有13项出现左心室质量显著降低，而在10项使用利尿剂或血管扩张剂的试验中仅有2项出现这种情况（平均值 = 7.11；p小于0.01）。然而，关于血管紧张素II降低程度和肾上腺素能效应、这些系统之间可能的相互作用以及心脏血流动力学负荷诱导变化的不完全特征等方面的不确定性，都限制了对现有研究的解释。初步数据表明，在原发性和继发性人类高血压中，肾素 - 血管紧张素系统活性与左心室收缩功能之间存在负相关关系，这一可能性值得进一步研究。
