Curr Hypertens Rep. 2009 Dec;11(6):412-20. doi: 10.1007/s11906-009-0071-0.
The pathologic hypertrophy of hypertensive heart disease is related to the quality, not the quantity, of myocardium; the presence of fibrosis is inevitably linked to structural and functional insufficiencies with increased cardiovascular risk. Elevations in plasma aldosterone that are inappropriate relative to dietary sodium, or relative aldosteronism, are accompanied by suppressed plasma renin activity, elevation in arterial pressure, and dyshomeostasis of divalent cations. The accompanying hypocalcemia, hypomagnesemia, and hypozincemia of aldosteronism contribute to the appearance of secondary hyperparathyroidism. Parathyroid hormone-mediated intracellular calcium overloading of cardiac myocytes and mitochondria leads to the induction of oxidative stress and molecular pathways associated with cardiomyocyte necrosis and scarring of myocardium, whereas the dyshomeostasis of zinc compromises antioxidant defenses. This dys-homeostasis of calcium and zinc, intrinsically coupling prooxidant calcium and antioxidant zinc, raises the prospect for therapeutic strategies designed to mitigate intracellular calcium overloading while enhancing zinc-mediated antioxidant defenses, thus preventing adverse myocardial remodeling with fibrosis, associated diastolic dysfunction, and cardiac arrhythmias.
高血压性心脏病的病理性心肌肥大与心肌的质量而非数量有关；纤维化的存在不可避免地与结构和功能不足以及心血管风险增加相关。血浆醛固酮升高与膳食钠相对或相对醛固酮症不适当，同时伴有血浆肾素活性抑制、动脉压升高和二价阳离子的动态平衡失调。醛固酮症的伴随低钙血症、低镁血症和低锌血症导致继发性甲状旁腺功能亢进的出现。甲状旁腺激素介导的心肌细胞和线粒体细胞内钙超载导致氧化应激和与心肌细胞坏死和心肌瘢痕形成相关的分子途径的诱导，而锌的动态平衡失调则损害抗氧化防御。钙和锌的这种动态平衡失调，内在地将促氧化剂钙和抗氧化锌耦合在一起，提出了旨在减轻细胞内钙超载的治疗策略的前景，同时增强锌介导的抗氧化防御，从而防止纤维化、相关舒张功能障碍和心律失常引起的不良心肌重构。
