Department of Cardiology, Tianjin Medical University General Hospital, Tianjin Medical University , Tianjin, China.
Department of Medical Cosmetology, Tianjin Medical University General Hospital, Tianjin Medical University , Tianjin, China.
Clin Exp Hypertens. 2020 Aug 17;42(6):531-538. doi: 10.1080/10641963.2020.1723615. Epub 2020 Feb 5.
Evidence indicates that renin-angiotensin-aldosterone system (RAS) inhibitors can protect the brain in Alzheimer's disease and Parkinson's disease. The current study evaluated the relationship between aldosterone and tissue damage in the brains of spontaneously hypertensive rats (SHRs) and whether the RAS inhibitor eplerenone can mitigate the damage seen in these rats. SHRs were randomly divided into eplerenone (n = 10) and SHR (n = 10) groups, and Wistar-Kyoto (WKY) rats (n = 10) were used as controls. Eplerenone 50 mg/kg/day was administered orally to the eplerenone group. Pathological changes to the hippocampal formation, plasma and encephalic aldosterone, and plasma potassium levels were compared among the groups. After 10 weeks, rats in the eplerenone and SHR groups showed higher systolic BP ( = .01) than the control group. Aldosterone levels in the brain were higher in the SHR group (0.20 ± 0.06 pg/ml) than in the eplerenone (0.14 ± 0.05 pg/ml, = .044) or control (0.12 ± 0.07 pg/ml, = .007) groups. Plasma aldosterone levels in the SHR group were 1.7 times higher than those in the control group ( = .006). Cerebral cortex was thinner in the SHR group (225.18 ± 15.43 μm) than in the eplerenone (240.38 ± 12.85 μm, < .01) or control (244.72 ± 18.92 μm, < .01) groups. Thickness did not differ between the latter two groups. The SHR group exhibited apoptotic cells in the hippocampal formation, which were rare in the eplerenone and control groups. Plasma potassium levels were higher in the eplerenone group than those in the other two groups ( < .05). Our results showed that eplerenone can alleviate brain damage (thinning of cortex and increased apoptosis) caused by aldosterone in a rat model of hypertension.
证据表明，肾素-血管紧张素-醛固酮系统（RAS）抑制剂可保护阿尔茨海默病和帕金森病患者的大脑。本研究评估了醛固酮与自发性高血压大鼠（SHR）脑组织损伤之间的关系，以及 RAS 抑制剂依普利酮是否能减轻这些大鼠的损伤。SHR 被随机分为依普利酮（n=10）和 SHR（n=10）组，Wistar-Kyoto（WKY）大鼠（n=10）作为对照组。依普利酮组每天口服 50mg/kg 依普利酮。比较各组海马结构的病理变化、血浆和脑内醛固酮以及血浆钾水平。10 周后，依普利酮组和 SHR 组大鼠的收缩压均高于对照组（ =0.01）。SHR 组大鼠脑内醛固酮水平（0.20±0.06pg/ml）高于依普利酮组（0.14±0.05pg/ml， =0.044）和对照组（0.12±0.07pg/ml， =0.007）。SHR 组大鼠血浆醛固酮水平是对照组的 1.7 倍（ =0.006）。与依普利酮组（240.38±12.85μm， <0.01）和对照组（244.72±18.92μm， <0.01）相比，SHR 组大鼠大脑皮质较薄（225.18±15.43μm， <0.01）。后两组之间厚度无差异。SHR 组海马区可见凋亡细胞，而依普利酮组和对照组少见。依普利酮组大鼠的血浆钾水平高于其他两组（ <0.05）。我们的研究结果表明，依普利酮可减轻高血压大鼠模型中醛固酮引起的脑损伤（皮质变薄和凋亡增加）。
