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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Angiotensin-Converting Enzyme Inhibitors, Animals, Aorta, Blotting, Western, Cardiomegaly, Denervation, Male, Peptidyl-Dipeptidase A, Rats, Rats, Sprague-Dawley, Real-Time Polymerase Chain Reaction, Renin-Angiotensin System.
user
Is angiotensin converting enzyme involved in the cardiac hypertrophy induced by sinoaortic denervation in rats? Context: The present study was designed to test the hypothesis that local angiotensin converting enzyme (ACE) was involved in the cardiac hypertrophy induced by sinoaortic denervation (SAD) in rats. Experiment 1: Six weeks after SAD of rats, components of renin-angiotensin system (RAS) in left ventricles were assayed by quantitative real-time PCR and Western blotting analysis. Experiment 2: Rats were divided into five groups treated as follows: (1) sham-operated group; (2) SAD group; (3) SAD group treated with angiotensin II type 1 receptor (AT1R) antagonist losartan (10 mg·kg(-1)·day(-1), orally); (4) SAD group treated by ACE inhibitor ramipril (1 mg·kg(-1)·day(-1), orally); (5) SAD group treated by ramipril and the B2-kinin receptor selective antagonist HOE-140 (0.25 mg·kg(-1)·day(-1), subcutaneously). SAD led to augmentation of the mRNA levels and protein expression of left ventricular ACE and AT1R. Both losartan and ramipril ameliorated SAD-induced left ventricular hypertrophy. Both losartan and ramipril abated oxidative stress, suppressed inflammation, and reduced expression TGFβ-R in left ventricles. In addition, the protective effect of ramipril could be abolished by HOE-140.
assistant
Local ACE is involved in the left ventricular hypertrophy induced by sinoaortic denervation in rats, via both angiotensin II/AT1R and bradykinin/B2R pathways. Final Decision: yes