Effects of moxonidine hydrochloride on left ventricular hypertrophy and c-myc gene expression in spontaneously hypertensive rats

Objective: To investigate the regression effect of domestic moxonidine hydrochloride on left ventricular hypertrophy and the potential mechanism of spontaneously hypertensive rats (SHR). Methods: Thirty male SHRs aged 20 weeks were randomly divided into Mox + SHR, Cap + SHR and SHR (10/group) groups. Ten age- and sex-matched sprauge-dawley rats were designed as normal control (NC). At the end of 13-week observation, the ratio of left ventricular weight/body weight (LVW/BW), collagen volume fraction (CVF), standardized perivascular collgen area (PVCA) and intramyocardial arterial average medial thickness (AMT) as well as c-myc gene expressiona (A) were assayed. Results: LVW/BW, CVF, PVCA, AMT and c-myc gene expression in group Mox + SHR were significantly lower than those in group SHR [LVW/BW (3.46±0.13)mg·g^-1 vs (3.96±0.18) mg·g^-1, CVF(0.086±0.018) vs (0.046±0.015), PVCA (0.69±0.11) vs (1.34±0.29), AMT(7.97±0.73) μm vs (11.9±11.16) μm, A (0.74±0.16) A vs (1.24±0.21)A, P<0.01]. Conclusion: Long-term antihypertensive treatment with moxonidine hydrochloride can reverse left, ventricular hypertrophy in SHR.