Goodfriend Theodore L
Department of Medicine, University of Wisconsin Medical School, Madison, WI, USA.
J Clin Hypertens (Greenwich). 2006 Feb;8(2):133-9. doi: 10.1111/j.1524-6175.2006.05110.x.
Aldosterone stimulates reabsorption of sodium, sustaining blood volume and pressure in the face of salt deprivation or extracellular fluid depletion. The steroid also stimulates excretion of potassium, protecting extracellular fluid from excessive levels of that ion. These two actions are relatively rapid and clearly adaptive when appropriately initiated and terminated, but maladaptive when prolonged or excessive, causing hypertension and electrolyte imbalance. Aldosterone and other mineralocorticoids exert slower, direct effects on cells in the heart, kidneys, and vessels, leading to hypertrophy, fibrosis, and dysfunction contributing to degenerative cardiovascular diseases. The maladaptive actions of aldosterone are exacerbated by sodium chloride, angiotensin, endothelin, and certain growth factors. Damage can be minimized by antagonists of aldosterone receptors, inhibitors of the renin system, depletion of salt, and repletion of potassium and magnesium. Specific inhibitors of fibrosis and hypertrophy, and more effective inhibitors of the renin system should be useful in the future.
醛固酮刺激钠重吸收，在盐缺乏或细胞外液减少时维持血容量和血压。这种类固醇激素还刺激钾排泄，保护细胞外液免受该离子过量水平的影响。这两种作用相对迅速，在适当启动和终止时明显具有适应性，但如果持续时间过长或作用过度则会产生适应不良，导致高血压和电解质失衡。醛固酮和其他盐皮质激素对心脏、肾脏和血管中的细胞产生较慢的直接影响，导致肥大、纤维化和功能障碍，进而引发退行性心血管疾病。氯化钠、血管紧张素、内皮素和某些生长因子会加剧醛固酮的适应不良作用。醛固酮受体拮抗剂、肾素系统抑制剂、减少盐分摄入以及补充钾和镁可将损害降至最低。纤维化和肥大的特异性抑制剂以及更有效的肾素系统抑制剂未来可能会发挥作用。
