INHIBITORY EFFECTS OF CAPTOPRIL ON C-MYC EXPRESSION DURING LEFT-VENTRICULAR HYPERTROPHY

AIM: To study the molecular mechanism of captopril (Cap) on the inhibi tion of left ventricular hypertrophy (LVH), disclose the expression an d distribution of c-myc in different cell types in left ventricle (LV) in spontaneously hypertensive rats (SHR). METHODS: Cap 100 mg . kg(-1 ) . d(-1) was given po to SHR. Systolic blood pressure (SBP), left ven tricular weight (LVW), and body weight (BW) were measured at 16-wk old . The level of angiotensin II (Ang II), c-myc mRNA, and oncoprotein we re determined by immunohistochemical method, Northern blot, and Wester n blot, respectively. RESULTS: Cap reduced SEP, LVW/BW in SHR, with a decrease of Ang II and c-myc expression in LV. Local cardial Ang II ma inly distributed in cardiomyocytes. Cap inhibited cardial Ang II produ ction and c-myc expression ( histochemical staining intensity index, 0 .49 +/- 0.04 vs 0.83 +/- 0.24, P < 0.01). The c-myc oncoprotein was pr evailingly located in cardiac fibroblasts. The c-myc oncoprotein in Ca p treated SHR was lower than that of WKY. CONCLUSION: High expression of c-myc in fibroblasts played an important role in the development of LVH in SHR. Inhibitory effects of Cap on LVH was associated with a de creased myocardial Ang II and interstitial fibroblasts c-myc expressio n. The c-myc oncoprotein post-transcriptional translation was also int errupted by Cap.