Weber K T, Sun Y, Campbell S E, Slight S H, Ganjam V K, Griffing G T, Swinfard R W, Diaz-Arias A A
Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, USA.
Steroids. 1995 Jan;60(1):125-32. doi: 10.1016/0039-128x(94)00030-g.
Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.
慢性盐皮质激素（MC）过量，无论其是由于血浆醛固酮（ALDO）升高还是脱氧皮质酮（DOC）升高所致，均与全身及冠状动脉小动脉的血管周围纤维化相关。这种阻力血管的重塑促成了高血压的出现。慢性MC过量还伴有心肌细胞坏死，这继发于心肌钾耗竭，随后在血压正常、未肥厚的右心室以及血压升高、肥厚的左心室中出现修复性纤维化。纤维化促成了室性心律失常和功能障碍的出现。本文展示了将循环中ALDO和DOC慢性、不适当（相对于饮食中的钠）升高与心脏及其他组织中这些反应性和修复性纤维组织形成形式相联系的临床和实验证据。
