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Objective: To investigate the effect of tanshinone II(A) on the expression of different components in the renin-angiotensin system of left ventricles of renal hypertensive rats., Method: The renal hypertension model was established in rats by the two-kidney-one-clip (2K1C) method. In the experiment, all of the rats were randomly divided into four groups (n = 15 per group) before the operation: the sham-operated (Sham) group, the hypertensive model (Model) group, the low-dose tanshinone II(A) group and the high-dose tanshinone II(A) group. At 5 week after the renal artery narrowing, the third and fourth groups were administered with 35 mg kg(-1) x d(-1) and 70 mg x kg(-1) x d(-1) of tanshinone II(A), respectively. The blood pressure in rats was determined by the standard tail-cuff method in each week after the operation. After the drug treatment for 8 weeks, all the rats were put to death, and their left ventricles were separated to determine the ratio of left ventricle weight to body weight (LVW/BW), the myocardial collagen content, and the expressions of different components in myocardial RAS, including angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin 1-type receptor (AT1R), Mas receptor mRNA expression and angiotensin II (Ang II) and angiotensin (1-7) [Ang (1-7)] content., Result: Compared with the sham group, the hypertensive model group exhibited a markable increase in the content of Ang II and Ang (1-7) and the mRNA expressions of ACE, ACE2, AT1R and Mas (P < 0.01). However, the treatment with tanshinone II(A) showed the does dependence, inhibited left ventricle hypertrophy, decreased myocardial Ang II content and the mRNA expression of ACE and AT, R in renal hypertensive rats (P < 0. 01) , further increased the myocardial Ang (1-7) content and the mRNA expression of ACE2 and Mas (P < 0.01) , but without any change in the blood pressure of hypertensive rats., Conclusion: The treatment with tanshinone II(A) could inhibit left ventricle hypertrophy of renal hypertensive rats. Its mechanism may be partially related to the expression of different components in the renin-angiotensin system for regulating myocardial tissues.

Objective: To investigate the efficacy of combined gene transfer of vascular endothelial growth factor (VEGF) and angiotensin-1 (Ang-1) in swine coronary artery occlusion., Methods: Swine underwent left thoracotomy followed by ligation of left anterior descending coronary artery. Constructed PCD(2)/VEGF and/or PCD(2)/Ang-1 eukaryotic expression plasmid was directly injected into the swine myocardium. RT-PCR, immunohistochemistry, capillary density and arteriole density were used to detect gene expression and biological effect. Coronary angiography was done to evaluate collateral circulation of the occluded artery., Results: High levels of VEGF and Ang-1 mRNA and protein expression were detected. There was a significant increase in the number of capillaries and arterioles as compared with a control group (P < 0.05). Capillary density and arteriole density of the combination therapy group were higher than those of the swing receiving either therapy alone. Coronary angiography showed better collateral circulation in the combination therapy group., Conclusions: Direct injection of PCD(2)/VEGF and PCD(2)/Ang-1 can transfect the myocardium and express VEGF and Ang-1 protein. Combined gene transfer of VEGF and Ang-1 can increase capillary and arteriole number and enhance collateral circulation of the occluded coronary artery more effectively.