Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B

Objective: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism. Methods: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls. Blood pressure was measured before the experiment and then once every week after the beginning of experiment. By the end of the experiment the rats were killed and their hearts were taken out to measure the left ventricle weight/body weight. RT-PCR was used to detect the mRNA expression of atrial natriuretic peptide (ANP) and of protein kinase B (PKB) in myocardium. Western blotting was used to examine the protein expression of PKB. Results: 1 The systolic blood pressure of the SHR normal control and treatment groups were 221 mm Hg ± 10 mm Hg and 217 mm Hg ± 8 mm Hg respectively (P > 0.05) and the systolic pressure of the normal control group was 126 ± 6 mm Hg, significantly lower than those of the 2 SHR groups (both P < 0.01). 2 The LVW/BW values of the SHR control group were 3.04 mg/g ± 0.12 mg/g, 3.73 mg/g ± 0.08 mg/g, and 4.10 mg/g ± 0.13 mg/g in the normal control group, SHR treatment group and SHR control group respectively with significant difference between any 2 groups (all P < 0.01). 3 The mRNA expression levels of ANP were 0.44 ± 0.33, 0.27 ± 0.03, and 0.17 ± 0.33 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). 4 The mRNA expression levels of PKB were 0.45 ± 0.05, 0.32 ± 0.03, and 0.19 ± 0.02 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). Conclusion: Simvastatin reverses LVH and myocyte phenocyte transformation in the SHRs with the possible mechanism of decreasing the expression level of PKB.