| It has been proved that the Left ventricular hypertrophy is not only a severe complication of essential hypertension, but also an important risk factor to heart failure. The proliferation of cardiac Fibroblasts(CFS) and the hypertrophy of myocardial cell is the vital pathophysiological bases which lead to Left ventricular hypertrophy. Though at the beginning myocardial hypertrophy is a beneficially compensatory adaptation reaction, persistent myocardial hypertrophy caused by chronic overload can result in the deterioration of heart function and finally dilated cardiomyopathy, followed by heart failure and sudden death. Therefore, how to improve and reverse left ventricular hypertrophy has become the focus in the treatment of essential hypertension . Urotension II (UII) is a recently identified vasoactive peptide, whose constriction effct on vessels is over 10 times stronger than endothelin-1, and it is one of most powerful vasoconstrictor in vivo identified to date.Besides its vasoconstictive effect, UII is also an important mitogen,which can promote the proliferation of vascular smooth muscle cells(VSMCs),CFS and airway smooth muscle cell. Among a lot of neurohumoral factors, the effect of UII oncardiomyocytes remains unknown at present. Statins, as potent lipid -regulating drugs, can not only lower strikingly serum cholesterin and low-density lipoprotein,but also have more effects which are beyond that of lipid -regulating , for example, inhibiting the proliferation of CFS and VSMC,preventing thrombosis and protecting endothelium. However, whether statins have influence on the hypertrophy of myocardial cell induced by UII and its related mechanism remain unknown, and therefore, need to be further investigated. The aim of our study is to observe the effects of UII on the hypertrophy of myocardial cell and the intervention effect of Atrovastin on the hypertrophy of myocardial cell induced by UII ,which can offer new theoretical evidence and also give a new conception for the prevention and treatment of Left ventricular hypertrophy.In this study, neonatal Sprague-Dawley(SD) rats were used as experiment object. Measurement of cell surface and FITC-conjugated phalloidin immunocytochemistry was adopted to evaluate the size of myocardial cell. Protein content and 3H-leucine incorporation in myocardial cell was used to assess protein synthesis and Laser Scanning Confocal Microscope(LSCM) was used to observe the change of calcium in the myocardial cell. All the methods were used to observe: (l)the effect of UII on the hypertrophy of myocardial cell; (2)the relation between UII and calcium ion;(3)how does ERKs signal pathway influence the myocardial cell hypertrophy induced by UII;(4)The intervention of Atrovatatin on the myocardial cell hypertrophy induced by UII.The results of the study showed that: (1) UII dose-dependently increased myocardial cell surface area, After 10-8 and 10-7mol/L UII were added, the cell surface areas were 2046.30+268.36um2 and 3662.2 +259.16 um2, respectively, both were significantly higher than that ofcontrol(both P<0.01) . (2)As UII concentration rose from 10-10 to 10-7mol/L,the protein content increased gradually.the protein content of 10-8and 10-7 mol/L UII groups were 1.597 +0.372 and 1.885 + 0.245 ng/cell,respectively, which are markedly higher than that of control (P<0.01).(3)the 3H-leucine incorporation in myocardial cell increased also in a dose dependent manner. H-leucine incorporation of 10-8 and 10-7 mol/L groups were 2508.33+299.81 and 2898.83+625.41 (cpm/well), respectively, They were both significantly higher than that of control (1026.83 +91.67cpm/well), (P<0.01). (4)Compared with control group, the enhanced microfibril organization can be seen in myocardial cell stimulated by 10-7 mol/L UII. (5)A rapid increase of calcium in myocardial cell was observed through LSCM after 1 X10-7 mol/L UII were added in myocardial cell immediately. Fluorescence intensity of calcium(99.01 + 14.09) was higher than that of control(34.58 + 5.80) (P<0.01), the density of calcium... |
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