Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Princess Alexandra and Greenslopes Hospitals, Brisbane, Australia.
Endocrinology. 2012 Nov;153(11):5137-42. doi: 10.1210/en.2012-1573. Epub 2012 Aug 23.
Corticosteroid excess is associated with adverse cardiovascular outcomes. Patients with Cushings's syndrome, either caused by endogenous or exogenous glucocorticoid excess, and patients with primary aldosteronism have increased cardiovascular risk. The increase in risk is mediated partly by traditional cardiovascular risk factors including hypertension and metabolic syndrome but also by other, less well-characterized mechanisms. Experimental and human studies have shown that target organ deterioration induced by aldosterone depends on concomitant high dietary salt intake. Key ongoing research questions that warrant further study by both clinical and experimental approaches include the following: 1) beyond inducing the metabolic syndrome, what are the mechanisms by which glucocorticoids are associated with excess cardiovascular risk, 2) what are the cellular pathways by which excessive mineralocorticoid receptor activation brings about cardiovascular and renal damage, and 3) why is salt critical in this process?
皮质醇过多与不良心血管结局相关。无论是内源性或外源性糖皮质激素过多引起的库欣综合征患者，还是原发性醛固酮增多症患者，其心血管风险均增加。风险增加部分是通过传统心血管危险因素（包括高血压和代谢综合征）介导的，但也有其他不太明确的机制。实验和人体研究表明，醛固酮引起的靶器官损害取决于同时的高盐饮食摄入。通过临床和实验方法进一步研究的关键待解决问题包括以下内容：1）除了引起代谢综合征之外，糖皮质激素与心血管风险增加有何关联的机制，2）过多的盐皮质激素受体激活引起心血管和肾脏损害的细胞途径是什么，3）为什么盐在这个过程中很关键？
