CHANGES IN MYOCARDIAL/RENAL/PULMONARY RENIN ANGIOTENSIN SYSTEMS IN HEART FAILURE

我们研究了局部肾素的各种成分的表达。 血管紧张素系统(RAS)定量测定心脏、肾脏、肺 肾素、血管紧张素转换酶(ACE)和 高血压大鼠血管紧张素II受体亚型(AT-1和AT-2)的变化 不同程度的充血性心力衰竭，由主动脉腔静脉的形成引起 瘘管(ACF)。大鼠要么代偿并维持正常的肥厚， 这在失代偿大鼠中更明显。肾脏肾素-mRNA增加52% 在代偿动物中为130%，在失代偿大鼠中为130%。肾素基因 大鼠心肌中的水平也增加了68%和140% 代偿性和失代偿性充血性心力衰竭。血管紧张素转换酶基因表达增加 心脏中也有类似的模式，但肾脏中没有。此外，肾脏 和心脏血管紧张素转换酶免疫反应性水平，用不同的方法评估 也表现出了同样的趋势。AT-1受体基因表达水平仅在 失代偿期大鼠心肌AT-2受体基因表达无明显变化 所研究的任何组织的变化。 因此，CHF与血管紧张素转换酶基因表达显著增加有关 心中的地方RAS。

We studied the expression of various components of the local renin- angiotensin system (RAS) by quantitation of cardiac, renal, an pulmonary mRNA levels of renin, angiotensin converting enzyme (ACE) and angiotensin II receptor subtypes (types AT-1 and AT-2) in rats with different severities of CHF, induced by the creation of an aortocaval fistula (ACF). Rats either compensate and maintain normal hypertrophy, which was greater in decompensated rats. Renal renin-mRNA increased 52% in compensated animals and 130% in decompensated rats. Renin mRNA levels in the myocardium also increased 68% and 140% in rats with compensated and decompensated CHF, respectively. ACE-mRNA increased in a similar pattern in the heart but not in the kidneys. Moreover, renal and cardiac ACE innumoreactivity levels, assessed by a different method showed the same trend. AT-1 recpetor mRNA levels decreased 54% only in the myocardium of decompensated rats, while AT-2 receptor mRNA did not change in any tissue studied. Thus, CHF is associated with a remarkable increase in the expression of the local RAS in the heart.