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对心血管具有保护作用的醛固酮受体拮抗剂依普利酮 总被引:1,自引:0,他引:1
目的:介绍一种新型的醛固酮受体拮抗剂依普利酮(eplerenone)对心血管的保护作用。方法:从临床有效性、安全性和药理学阐述依酱利酮在心血管疾病中的作用。结果:依普利酮能有效降低血压,减轻心血管内皮损伤,减少危险事件和终点事件的发生.与螺内酯相比不良反应小。结论:临床医师应重视选择性醛固酮受体拮抗剂在治疗心血管疾病中的应用。 相似文献
3.
近年来多项动物和临床研究已证实醛固酮对心血管系统有多种毒性作用 ,在心力衰竭的病理生理过程中起重要作用 ,醛固酮在高盐和高血管紧张素Ⅱ状态下可引起心肌纤维化 ,且这一作用独立于其致高血压作用。醛固酮可诱导多种血管炎症反应 ,可能有致急性心肌梗死作用 ,并可能在急性心肌梗死后的心室重构中起重要作用。已有多项大型临床试验证明醛固酮受体拮抗剂能明显降低心力衰竭病人的死亡率。埃普利酮对醛固酮受体的选择性大大高于安体舒通 ,所以其激素样不良反应发生率明显低于安体舒通 ,而同样能对心力衰竭病人起保护作用。 相似文献
4.
Yosuke Omori Toshiaki Mano Tomohito Ohtani Yasushi Sakata Yasuharu Takeda Shunsuke Tamaki Yasumasa Tsukamoto Takeshi Miwa Kazuhiro Yamamoto Issei Komuro 《Yonago acta medica》2014,57(3):109-116
Background
Cardiac fibrosis is considered to be a crucial factor in the development of heart failure. Blockade of the mineralocorticoid receptor (MR) attenuated cardiac fibrosis and improved the prognosis of patients with chronic heart failure but the ligand for MR and the regulatory mechanism of MR pathway in the diseased heart are unclear. Here, we investigated whether glucocorticoids can promote cardiac fibrosis through MR in oxidative stress and the involvement of elongation factor eleven-nineteen lysine-rich leukemia (ELL), a co-activator of MR, in this pathway.Methods and Results
The MR antagonist eplerenone attenuated corticosterone-induced collagen synthesis assessed by [3H]proline incorporation in rat neonatal cultured cardiac fibroblasts in the presence of H2O2, as an oxidative stress but not in the absence of H2O2. H2O2 increased the ELL expression levels and MR-bound ELL. ELL expression levels and MR-bound ELL were also increased in the left ventricle of heart failure model rats with significant fibrosis and enhanced oxidative stress. Eplerenone did not attenuate corticosterone-induced increase of [3H]proline incorporation in the presence of H2O2 after knockdown of ELL expression using small interfering RNA in cardiac fibroblasts.Conclusion
Glucocorticoids can promote cardiac fibrosis via MR in oxidative stress, and oxidative stress modulates MR response to glucocorticoids through the interaction with ELL. Preventing cardiac fibrosis by modulating glucocorticoid-MR-ELL pathway may become a new therapeutic strategy for heart failure. 相似文献5.
6.
《Expert opinion on pharmacotherapy》2013,14(4):509-515
The aim of this prospective, randomised, open-label, blinded-end point study was to compare the efficacy and safety of eplerenone versus spironolactone in patients with bilateral idiopathic hyperaldosteronism (IHA). After a 2-week washout period, 34 patients with IHA were assigned to receive either spironolactone 25 mg b.i.d. (n = 17) or eplerenone 25 mg b.i.d. (n = 17) for 24 weeks. If the patients' blood pressure (BP) was not < 140/90 mmHg, the doses were gradually increased up to 400 mg for spironolactone and 200 mg for eplerenone. If the patients' BP remained uncontrolled, a daily dose of hydrochlorothiazide 12.5 mg was added at week 16. The primary outcome was the percentage of patients with BP < 140/90 mmHg at 16 weeks (i.e., with aldosterone antagonist monotherapy). The patients' BP was normalised in 13 out of 17 (76.5%) and 14 out of 17 (82.4%) patients in the spironolactone and eplerenone groups, respectively (p = 1.00). Systolic BP decreased more rapidly with eplerenone. Serum potassium levels were normalised (> 3.5 mmol/l) in all patients at 4 weeks. Mild hyperkalaemia was observed in two patients receiving 400 mg of spironolactone and in three patients receiving 150 mg of eplerenone. Two patients presented with bilateral painful gynaecomastia at the end of week 16 while receiving 400 mg of spironolactone. Switching spironolactone to 150 mg of eplerenone daily resulted in resolution of gynaecomastia and also maintained BP control. At the end of the study, 19 patients were on eplerenone and 15 were on spironolactone. However, this did not affect the primary end point, because the switch from spironolactone to eplerenone (in two patients) occurred at the end of week 16. It was concluded that eplerenone was as effective as spironolactone in reducing BP in patients with IHA. The risk of mild hyperkalaemia was similar with both drugs. 相似文献
7.
Quinkler M Stewart PM 《Best Practice & Research: Clinical Endocrinology & Metabolism》2010,24(6):923-932
The prevalence of primary hyperaldosteronism approaches 10% of?all hypertensive patients, and besides efficient diagnostic procedures, effective treatment is of increasing importance to reverse increased morbidity and mortality. Aldosterone-producing adenoma and unilateral adrenal hyperplasia are amenable to cure?by endoscopic adrenalectomy. Bilateral adrenal hyperplasia (micro- or macronodular), which comprises two-thirds of primary hyperaldosteronism, is treated primarily by mineralocorticoid receptor antagonists (starting dose 12.5-25mg/day spironolactone with titration up to 100mg/day, alternatively 50-100mg/day eplerenone). If blood pressure is not normalised by this first-line treatment, additional treatment with potassium-sparing diuretics (amiloride or triamterene) or calcium channel antagonists is necessary. The start of medication should be closely monitored by serum electrolyte and creatinine controls. 相似文献
8.
目的:探讨依普利酮对阿霉素诱导心衰大鼠血清TNF-α的影响及其治疗心衰的可能机制。方法:50只雄性SD大鼠随机挑选40只腹腔注射阿霉素制做心衰模型,其余10只作为正常对照组。6周后将存活的20只模型鼠随机分为2组:心力衰竭+依普利酮治疗组(n=10),给予依普利酮200mg/(kg.d)灌胃,心力衰竭组(n=10)与正常对照组大鼠(n=10)给与安慰剂(生理盐水)灌胃,12周后观测一般变化,测定大鼠心功能及血清TNF-α含量。结果:心衰组血流动力学指标与正常组相比有显著性差异(P〈0.05)。治疗组血流动力学指标与心衰组相比有显著性差异(P〈0.05)。心衰组TNF-α水平与正常组相比明显升高(P〈0.05)。治疗组TNF-α水平与心衰组相比明显下降,有显著性差异(P〈0.05)。结论:依普利酮可以降低心衰大鼠血清TNF-α的含量。 相似文献
9.
Akira Nishiyama Hirofumi Hitomi Asadur Rahman Hideyasu Kiyomoto 《Journal of pharmacological sciences》2009,109(1):1-6
There is increasing evidence demonstrating that the renoprotective effects of mineralocorticoid receptor (MR) blockade are independent of the effects exerted by renin-angiotensin inhibitors. MR is expressed not only in tubular cells but also in other renal cells including glomerular mesangial cells, podocytes, and renal interstitial fibroblasts. Animal experiments have shown that MR blockers prevent aldosterone-induced proteinuria, glomerular injury, and tubulointerstitial fibrosis. In vitro studies have also demonstrated that MR blockers inhibit aldosterone-induced renal cell damage. Recent clinical studies have shown that treatment with MR blockers attenuates the development of proteinuria in patients with chronic kidney disease (CKD) and hypertension, independent of changes in blood pressure. In some cases, MR blockers elicit potent renoprotective effects in conditions where aldosterone levels are not elevated. These data suggest that treatment with MR blockers may possibly present an effective therapeutic strategy for patients with CKD. 相似文献
10.
醛固酮腺瘤模型大鼠主动脉平滑肌细胞增殖与mdm2和p53的表达 总被引:1,自引:1,他引:0
目的 初步探讨肾上腺醛固酮腺瘤血管重构的机制.方法 将微量渗透泵植入大鼠皮下,随机分为对照组、腺瘤组、腺瘤+依普利酮组和腺瘤+肼苯哒嗪组.8周后检测主动脉平滑肌细胞的增殖状态和mdm2、p53的表达.结果 ①成功建立大鼠醛固酮腺瘤模型;②与对照组相比,腺瘤组大鼠主动脉平滑肌细胞增生活跃(P<0.05);MDM2 mRNA和蛋白表达上调(P<0.05);而p53只在蛋白水平增加(P<0.05);③相较于肼苯哒嗪,依普利酮能抑制醛固酮的作用(P<0.05).结论 醛固酮通过诱导mdm2表达而逆转p53的细胞周期阻滞作用,促使平滑肌细胞增殖,可能是醛固酮腺瘤血管重构的原因之一. 相似文献