| Myocardial hypertrophy is response to intrinsic or extrinsic stimulations. Recently, many studies show that many neural and humoral factors participate in hypertension-induced myocardial hypertrophy,especially the renin-angiotensin-aldosterone system (RAAS). Now, we realized that aldosterone is one of the most important factors in myocardial hypertrophy. But its detail mechanism has been still unclear. It has been shown that calcineurin-dependent signal-pathway may play an important role in the development of myocardial hypertrophy. Meanwhile, intrinsic calcineurin-inhibitor (Cain) had been proved of that can inhibit calcineurin-induced myocardial hypertrophy in vitro. It will be worthy of studyingwhether calcineurin-dependent signal-pathway is involved in the myocardial hypertrophy induced by aldosterone, and the expression of Cain and its significances in preventing myocardial hypertrophy.In our study, we made two myocardial hypertrophic animal models. One, by the way of aldosterone injected hypodermically, 28 wistar rats were divided into four groups randomly, control group, group of aldosterone injected, and groups of spironolactone or cyclosporin A injected separately. The other, by the operation of "one kidney one clip" (lklc), we successfully made a renovascular hypertensive model. 28 wistar rats were divided into four groups randomly, sham operation group, lklc group, and groups interfered with spironolactone or cyclosporin A separately. Two weeks later, we measured the blood pressure (BP) of the rats in two models. The level of aldosterone, angiotensin II and neuropeptide Y in plasma were determined by radioimmunoassay also. And caculating the ratio of heart weight to body weight (HW/BW) and leftventricular weight to body weight (LVW/BW). The expression of Cain in myocardium was observed by immunohistochemical staining, and estimated by western blot.We found that, in aldosterone injected model, the level of BP, HW/BW and LVW/BW, and the concentration of aldosterone in the plasma, all increased markedly (p<0.05) in aldosterone group. By immunohistochemical staining, we could find that positive pellet of Cain in myocardium increased in aldosterone group, and further observation showed that the expression of Cain obviously increased (p<0.05) by western blot, compared with control group. And, the results of the groups interfered with spironolactone or cyclosporin A showed that, the ratio of HW/BW and LVW/BW decreased, the level of aldosterone and neuropeptide Y in plasma increased significantly (p<0.05), and the expresion of Cain in myocardium markedly reduced (p<0.05).Also, in 1klc renovascular hypertensive rats, wefound that the level of BP, the ratio of HW/BW and LVW/BW, and the concentration of aldosterone and angiotensin II, all distinctly increased (p<0.05) in 1klc group, compared with sham operation group. Also the expression of Cain in myocardium notably increased by means of immunohistochemical staining or western blot in lklc group (p<0.05). While, in groups interfered with spironolactone or cyclosporin A, the ratio of LVW/BW, and the level of angiotensin II in plasma decreased markedly (p<0.05), meanwhile the concentration of neuropeptide Y became much higher (p<0.05), and the expression of Cain decreased significantly (/?<0.05), compared with lklc group.So, we can testify that whether extrinsic or intrinsic aldosterone levelup, may induce myocardial hypertrophy through a calcineurin-dependent signal-pathway. The expression of Cain in myocardium, a negative control protein in the rats, is related to the activity of calcineurin. By means of blocking the combination of aldosterone to its receptor,...
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