Stiefel P, Vallejo-Vaz A J, García Morillo S, Villar J
Unidad clínico-experimental de Riesgo Vascular (UCERV-UCAMI), IBIS. Hospital Universitario Virgen del Rocío, SAS, Universidad de Sevilla, CSIC Avenida, 41011 Sevilla, Spain.
Int J Hypertens. 2011;2011:685238. doi: 10.4061/2011/685238. Epub 2011 Jun 23.
Aldosterone facilitates cardiovascular damage by increasing blood pressure and through different mechanisms that are independent of its effects on blood pressure. In this respect, recent evidence involves aldosterone in the pathogenesis of metabolic syndrome. Although this relationship is complex, there is some evidence suggesting that different factors may play an important role, such as insulin resistance, renin-angiotensin-aldosterone system, oxidative stress, sodium retention, increased sympathetic activity, levels of free fatty acids, or inflammatory cytokines and adipokines. In addition to the classical pathway by which aldosterone acts through the mineralocorticoid receptors leading to sodium retention, aldosterone also has other mechanisms that influence cardiovascular tissue remodelling. Finally, overweight and obesity promote the adrenal secretion of aldosterone, increasing the predisposition to type 2 diabetes mellitus. Further studies are needed to better establish therapeutic strategies that act on the blockade of mineralocorticoid receptor in the treatment and prevention of cardiovascular diseases related to the excess of aldosterone and the metabolic syndrome.
醛固酮通过升高血压以及通过与其对血压的影响无关的不同机制促进心血管损伤。在这方面,最近的证据表明醛固酮参与代谢综合征的发病机制。尽管这种关系很复杂,但有一些证据表明不同因素可能起重要作用,如胰岛素抵抗、肾素 - 血管紧张素 - 醛固酮系统、氧化应激、钠潴留、交感神经活性增加、游离脂肪酸水平、炎症细胞因子或脂肪因子。除了醛固酮通过盐皮质激素受体起作用导致钠潴留的经典途径外,醛固酮还有其他影响心血管组织重塑的机制。最后,超重和肥胖会促进肾上腺分泌醛固酮,增加患2型糖尿病的易感性。需要进一步研究以更好地制定作用于盐皮质激素受体阻断的治疗策略,用于治疗和预防与醛固酮过多和代谢综合征相关的心血管疾病。