他汀类药物确实可减少心血管死亡率，并且似乎这种益处是独立于降脂治疗特性的。多国学者近期评估了他汀类药物是否可调节醛固酮的分泌，后者可导致心血管疾病。结果表明，高血压和188bet在线平台网址 患者应用他汀与醛固酮分泌减少有关，这一影响似乎在使用亲脂性他汀和较大剂量应用者中最为明显。相关论文近期发表于《循环》(Circulation)杂志。

        研究者们对两项干预试验中的受试者检测了肾上腺激素。在第一项试验的高血压受试者中，分析其基线以及高钠和低钠饮食后血管紧张素-II刺激后的醛固酮水平(1122个观察对象，15%接受为期3个月的他汀类药物治疗)。结果显示，在校正模型中，他汀使用者的醛固酮水平低了33%(P< 0.001)。皮质醇水平不受他汀影响。在次要分析中，亲脂性他汀和较大剂量他汀使用者的醛固酮水平最低。他汀使用者的血压较低，且血压的盐敏感性减少(P=0.001)。

        在第二项研究中，研究者们检测了高盐饮食188bet在线平台网址 患者血管紧张素-II刺激后的醛固酮水平(143个观察对象，79%是他汀类药物使用者)。研究结果再次证明他汀使用者的醛固酮水平较低(低了26%，P=0.006)，尤其是那些用亲脂性他汀者。

        大鼠肾上腺球状带细胞的体外研究也再次验证了亲脂性他汀可强烈抑制醛固酮，而不抑制皮质酮。

        参考文献：Rene Baudrand,et al. CIRCULATIONAHA.115.016759Published online before print October 2, 2015,doi: 10.1161/CIRCULATIONAHA.115.016759

Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects
1. Rene Baudrand1*;
2. Luminita H. Pojoga2;
3. Anand Vaidya2;
4. Amanda E. Garza2;
5. Paul A. Vöhringer3;
6. Xavier Jeunemaitre4;
7. Paul N. Hopkins5;
8. Tham M. Yao2;
9. Jonathan Williams2;
10. Gail K. Adler2;
11. Gordon H. Williams2
-Author Affiliations
1. 1Brigham and Women's Hospital, Harvard Medical School, Boston, MA & School Of Medicine, Pontificia Universidad Catolica De Chile, Santiago, Chile
2. 2Brigham and Women's Hospital, Harvard Medical School, Boston, MA
3. 3Hospital Clinico, FacultadMedicina Universidad de Chile, Santiago, Chile and Tufts Medical Center, Tufts University School of Medicine, Boston, MA
4. 4Centre Investigation Clinique, HôpitalEuropéen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Universite Paris Descartes, Paris, France
5. 5University of Utah School of Medicine, Salt Lake City, UT
1. ↵* Dept of Endocrinology, School Of Medicine, Pontificia Universidad Catolica De Chile, Santiago 8330074, Chile rbaudran@uc.cl
Abstract
Background—Statins substantially reduce cardiovascular mortality and appear to have beneficial effects independent of their lipid lowering properties. We evaluated the hypothesis that statin use may modulate the secretion of aldosterone, a well-known contributor to cardiovascular disease.
Methods and Results—We measured adrenal hormones in two intervention studies. In study 1 in hypertensive subjects, aldosterone was analyzed at baseline and after angiotensin-II stimulation (AngII) on both high (HS) and low sodium (LS) diets (1122 observations, 15% on statins > 3 months). Statin users had 33% lower aldosterone levels in adjusted models (p < 0.001). Cortisol was not modified by statins. In secondary analyses, the lowest aldosterone levels were seen with lipophilic statins and with higher doses. Statin users had lower blood pressure (BP) and reduced salt sensitivity of BP (p=0.001). In study 2, aldosterone was measured in diabetic patients on a HS diet, before and after AngII stimulation (143 observations, 79% statin users). Again, statin users had 26% lower aldosterone levels (p =0.006), particularly those using lipophilic statins. Ex vivo studies in rat adrenal glomerulosa cells confirmed that lipophilic statins acutely inhibited aldosterone, but not corticosterone, in response to different secretagogues.
Conclusions—Statin use among hypertensive and diabetic subjects was associated with lower aldosterone secretion in response to AngII and LS diet in two human intervention studies. This effect appeared to be most pronounced with lipophilic statins and higher doses. Future studies to evaluate whether aldosterone inhibition may partially explain the robust cardioprotective effects of statins are warranted.