摘要
目的:探讨缬沙坦、雷米普利及氨氯地平对自发性高血压大鼠(SHR)左室心肌中瞬时受体通道蛋白C亚族3及6(TRPC3及TRPC6)表达的影响。方法:将24只12周龄SHR大鼠随机分为4组,即SHR组、缬沙坦组、雷米普利组及氨氯地平组,每组6只。另以6只同龄的Wistar Kyoto大鼠(WKY)为正常对照组。给药4周后,检测各组大鼠的血压、左室质量指数、左室心肌细胞横径;RT-PCR及Western Blot检测TRPC3及TRPC6 mRNA及其蛋白的表达。结果:SHR组血压、左室质量指数及左室心肌细胞横径均明显高于对照组(P<0.05),3个药物组上述指标均较SHR组降低(P<0.05);5个组均有TRPC3及TRPC6的表达,SHR组TRPC3及TRPC6 mRNA及其蛋白的表达显著高于对照组(P<0.05),3个药物组TRPC3 mRNA及TRPC6 mRNA及其蛋白的表达均显著低于SHR组(P<0.05),缬沙坦组TRPC3 mRNA及其蛋白表达的减少最显著(P<0.05);3个药物组TRPC6 mRNA及其蛋白的表达有所下降,但组间比较差异无显著性。结论:SHR组及对照组大鼠均有TRPC3及TRPC6的表达,TRPC3及TRPC6可能共同参与调节心肌肥厚的病理生理过程;缬沙坦可能通过抑制TRPC3蛋白的表达参与逆转左室肥厚的过程。
AIM： To investigate the effect of valsartan, ramipril and anlodipine on the expression of TR- PC3 and TRPC6 in the left ventricle in spontaneously hypertensive rats （SHR）. METHODS： Twelve- week-old SHRs were randomly divided into four groups： valsartan-treated group （Val）, ramipril-treated group （Ram） , amlodipine-treated group （Aml） and untreated group （SHR）. Twelve-week-old Wistar- Kyoto （WKY） rats were used as control group. After 4 weeks of drug intervention, blood pressure （BP） , left ventricular mass index （LVMI） , left ventricular cardiomyocytes transection diameter （LVT- DM） were examined, RT-PCR and Western blotting were used to detect the expressions of TRPC3 and TRPC6 mRNA and protein. RESULTS： Compared with those in WKY, BP, LVMI and LVTDM in SHR were significantly higher （ P 〈 0. 05 ） and the data mentioned above decreased significantly in the drug intervention groups （P 〈 0. 05）. Expressions of TRPC3 and TRPC6 mRNA and protein were detected in each group and were significantly higher compared with those in WKY. TRPC3 decreased dramatically in drug intervention groups （P 〈 0. 05 ） and TRPC3 mRNA and protein decreased significantly in Val group compared with those in Ram group and Aml group. TRPC6 mRNA and protein expressions decreased in drug intervention groups; however, no significant changes in TRPC6 mRNA and protein expressions were observed. CONCLUSION： Expressions of TRPC3 and TRPC6 were found in SHR and WKY. TRPC3 and TRPC6 may co-regulate the pathphysiological processes of myocardial hypertrophy. Valsartan may inhibit left ventricular hypertrophy, probably by downregulating mRNA and protein expression of TRPC3.
出处
《心脏杂志》
CAS
2011年第4期459-464,共6页
Chinese Heart Journal
