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首页> 外文期刊>American Journal of Physiology >Chronic hyperaldosteronism in a transgenic mouse model fails to induce cardiac remodeling and fibrosis under a normal-salt diet.
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Chronic hyperaldosteronism in a transgenic mouse model fails to induce cardiac remodeling and fibrosis under a normal-salt diet.

机译：在正常盐饮食下，转基因小鼠模型中的慢性醛固酮增多症无法诱导心脏重塑和纤维化。

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Primary aldosteronism causes severe hypertension in humans (Conn's syndrome) with cardiac hypertrophy, characterized by a fibrosis more severe than the one observed in patients with essential hypertension. This suggests that aldosterone by itself may have specific and direct effects on cardiac remodeling through the activation of the cardiac mineralocorticoid receptor. Experimental evidence obtained in studying uninephrectomized rats treated with aldosterone or deoxycorticosterone (DOC) together with salt loading has led to similar conclusions. To examine the direct consequences of chronically elevated aldosterone levels on cardiac pathophysiology, we analyzed a mouse model (alpha-epithelial Na channel -/-Tg) that is normotensive under normal-salt diet but exhibits chronic hyperaldosteronism. Sixteen-month-old transgenic rescue mice that were kept under a regular salt diet that contains a small amount of sodium (0.3% Na(+)) displayed a compensated PHA-1 phenotype with normal body weight, normal kidney index, normal blood pressure, but 6.3-fold elevated plasma aldosterone levels compared with the age-matched control group. Peripheral resistance of distal colon to aldosterone was shown by a significant decrease of the amiloride-sensitive rectal potential difference, and its diurnal cyclicity was blunted. Despite chronically high plasma aldosterone levels, these animals do not show any evidence of cardiac hypertrophy, remodeling, or fibrosis, using collagen staining and anti-alpha-skeletal and alpha-smooth actin immunochemical labeling of heart sections. Cardiac fibrosis as seen in DOC- or aldosterone/salt-treated animal models is therefore likely to be due to the synergistic effect of salt, aldosterone, and other confounding factors rather than to the elevated circulating aldosterone levels alone.
机译：原发性醛固酮增多症会导致人的心脏肥大，引起严重的高血压（康氏综合症），其特征是纤维化的程度比在原发性高血压患者中观察到的严重。这表明醛固酮本身可能通过激活心脏盐皮质激素受体而对心脏重构产生特异性和直接的影响。在研究用醛固酮或脱氧皮质酮（DOC）以及盐负荷治疗的未切除直肠的大鼠中获得的实验证据得出了相似的结论。为了检查醛固酮水平长期升高对心脏病理生理学的直接影响，我们分析了正常盐饮食下血压正常但表现出慢性醛固酮增多症的小鼠模型（α-上皮Na通道-/-Tg）。在含有少量钠（0.3％Na（+））的常规盐饮食下饲养的16个月大转基因抢救小鼠表现出正常体重，正常肾脏指数，正常血压的PHA-1补偿表型，但血浆醛固酮水平比年龄匹配的对照组高6.3倍。阿米洛利敏感的直肠电位差的显着降低显示了远端结肠对醛固酮的外周抵抗，并且其昼夜周期性减弱。尽管血浆醛固酮水平长期居高不下，但使用胶原蛋白染色以及心脏切片的抗α-骨骼肌和α-平滑肌动蛋白免疫化学标记法，这些动物并未显示出任何心脏肥大，重塑或纤维化的迹象。因此，在DOC或醛固酮/盐治疗的动物模型中看到的心脏纤维化很可能是由于盐，醛固酮和其他混杂因素的协同作用所致，而不是单独的循环醛固酮水平升高。

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