RESUMO
The present study was performed to determine whether or not that cardiacrenin-angiotensin system (RAS) plays an important role in volume-overload myocardialhypertrophy. In order to control the increase of circulating RAS, aortacava fistula withnephrectomy (ACF+NT) rats were used in the experiment. The ventricular angiotensin Ⅰ,Ⅱ (Ang Ⅰ,Ⅱ) contents and angiotensin-converting enzyme (ACE) activities were measuredby means of radioimmunoassay and biochemical method. It was shown that in ACF+NTrats, the Ang Ⅱ contents and ACE activities in both left and right ventricles increasedsignificantly despite the plasma Ang Ⅰ, Ⅱ and renin activity remained at a lower level.These results indicate that: (1) Cardiac RAS as a relatively independent system, plays aregulatory role in the development of volume-overload cardiac hypertrophy; (2) The in-crease of Ang Ⅱ content was partly caused by the enhancement of ACE activities; (3) Atleast at the early stage of volume-overload cardiac hypertrophy, the circulating RAS maynot be a necessary promoter.
RESUMO
We studied the alteration of local and circulat-ing RAS during cardiac hypertrophy caused by ab-dominal aorta constriction (AC, with nephrectomyof left side) and aorta-vena fistula (AVF). Bothventricular and plasma angiotensin Ⅰ and Ⅱ (AngⅠ. Ⅱ), and plasma, renin actvity (RA) weremeasured by means of radioimmunoassay after twoand seven weeks of surgery. Despite the level ofplasma Ang Ⅰ, Ⅱ and RA were not enhanced, theventricular Ang Ⅰ and Ⅱ were increased signifi-cantly in AC rats (v. s. SO group P