RESUMO
This experiment on rats was aimed to investigate the expression of intermedin (IMD) in hypertrophic cardiac myoctye of renal vascular hypertension induced by incomplete ligation of the left renal artery, and so to detect and compare the changes of the expression after administration of Valsartan, Amlodipine and Enalapril respectively. The criterion for standard modeling was systolic pressure > or = 140 mmHg. At 4 weeks after successful modeling, 60 SD male rats were randomly divided into 5 groups, namely the hypertrophy group, the 3 drug-treatment groups, and the sham-operation group as control. Blood pressure, left ventricular mass index (LVMI), and the left ventricular mean transverse diameter of myocardial cell (LVTDM) were investigated at the 10th week after model establishment. Gene expression of IMD mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR), and the optical density of the band was measured by use of the Gel Documentation System. The ratio of IMD mRNA to beta-actin mRNA was considered the relative amount of IMD. When compared with control, the blood pressure increased significantly in the hypertrophy group. There was no statistically significant difference between the treatment groups. No significant difference in heart rate was noted at 4 weeks after operation in all groups. LVMI and LVTDM levels were significantly higher in the hypertrophy group than in the other groups; LVMI and LVTDM levels showed no significant difference among the treatment groups but they were obviously higher than those of the Sham-operation group. The gene expression of IMD mRNA in the hypertrophy group was upregulated in the myocardium, when compared with that in the other groups. Meanwhile, although IMD mRNA in the treament groups was higher than that in the Sham-operation group, no statistically significant difference of myocardial IMD mRNA was found between the treament groups. These results suggested that, in this experiment, intracardiac IMD mRNA was upregulated and could participate in the regulation of cardiac remodeling in renal vascular hypertension-induced cardiac hypertrophy. This upregulation could improve the pathologic and physiologic process of cardiac hypertrophy, and could associate with the pressure loading or myocardia hypertrophy. However, the change did not display any difference that could be attributed to the variety of hypotensive drugs.