Cardiac Renin-Angiotensin System in the Hypertrophied Heart

Abstract

Background The cardiac renin-angiotensin system (RAS) has been suggested to play an important role in heart failure and cardiac hypertrophy. In the present study, we evaluated the expression of each component of the RAS in hypertrophied heart induced by aortocaval shunt. Methods and Results The expression levels of renin, angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin II type Ia and Ib receptor (AT1aR and AT1bR) mRNA were determined by the reverse transcription–polymerase chain reaction method owing to the relatively low expression levels of these mRNAs in the ventricle. The expression level of renin or angiotensinogen mRNA in the ventricle was very low, more than 1000-fold lower than that in the kidney or liver, respectively. The expression of ACE mRNA in the ventricle was relatively abundant and was increased in the hypertrophied ventricle in this model, whereas no significant increases in the expression levels of AT1aR and AT1bR mRNA were observed. Administration of lisinopril attenuated the development of left and right ventricular hypertrophy in this model and was accompanied by an attenuation of the upregulation of the ACE, collagen type I-α, and vimentin mRNAs. Because the activity of the circulating RAS in the aortocaval shunt rats was not higher than that in the sham-operated rats, the effects of lisinopril in attenuating the ventricular hypertrophy may be due to inhibition of the increased ACE in the ventricle. Conclusions The present study supports the importance of ACE expressed in the ventricle in the development of hypertrophy induced by aortocaval shunt.