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）通过定量心脏、肾脏、肺 肾素、血管紧张素转换酶（ACE）和 血管紧张素II受体亚型（AT-1和AT-2型）在大鼠 不同严重程度的CHF，由创建下腔静脉引起 瘘管（ACF）。 大鼠要么补偿并维持正常的肥大， 在失代偿大鼠中更高。 肾组织肾素mRNA增加52% 在代偿期动物和失代偿期大鼠中分别为130%和130%。 肾素mRNA 心肌中的水平也增加了68%和140%， 分别为代偿性和失代偿性CHF。 ACE-mRNA表达增加， 心脏也有类似的情况但肾脏没有 此外，肾 和心脏ACE免疫反应性水平，通过不同的方法评估 显示出同样的趋势。 AT-1受体mRNA水平仅下降54%， 失代偿大鼠心肌AT-2受体mRNA表达无明显变化 任何研究组织的变化。 因此，CHF与以下蛋白表达的显著增加相关： 心脏的局部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.