Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria.
Cardiovasc Res. 2012 Apr 1;94(1):10-9. doi: 10.1093/cvr/cvs092. Epub 2012 Feb 13.
Animal and human studies support a clinically relevant interaction between aldosterone and parathyroid hormone (PTH) levels and suggest an impact of the interaction on cardiovascular (CV) health. This review focuses on mechanisms behind the bidirectional interactions between aldosterone and PTH and their potential impact on the CV system. There is evidence that PTH increases the secretion of aldosterone from the adrenals directly as well as indirectly by activating the renin-angiotensin system. Upregulation of aldosterone synthesis might contribute to the higher risk of arterial hypertension and of CV damage in patients with primary hyperparathyroidism. Furthermore, parathyroidectomy is followed by decreased blood pressure levels and reduced CV morbidity as well as lower renin and aldosterone levels. In chronic heart failure, the aldosterone activity is inappropriately elevated, causing salt retention; it has been argued that the resulting calcium wasting causes secondary hyperparathyroidism. The ensuing intracellular calcium overload and oxidative stress, caused by PTH and amplified by the relative aldosterone excess, may increase the risk of CV events. In the setting of primary aldosteronism, renal and faecal calcium loss triggers increased PTH secretion which in turn aggravates aldosterone secretion and CV damage. This sequence explains why adrenalectomy and blockade of the mineralocorticoid receptor tend to decrease PTH levels in patients with primary aldosteronism. In view of the reciprocal interaction between aldosterone and PTH and the potentially ensuing CV damage, studies are urgently needed to evaluate diagnostic and therapeutic strategies addressing the interaction between the two hormones.
动物和人体研究支持醛固酮和甲状旁腺激素 (PTH) 水平之间存在临床相关的相互作用，并表明这种相互作用对心血管 (CV) 健康有影响。本综述重点介绍了醛固酮和 PTH 之间双向相互作用的背后机制及其对心血管系统的潜在影响。有证据表明，PTH 可直接通过激活肾素-血管紧张素系统，以及间接通过激活肾素-血管紧张素系统，增加醛固酮从肾上腺的分泌。醛固酮合成的上调可能导致原发性甲状旁腺功能亢进患者的动脉高血压和心血管损害风险增加。此外，甲状旁腺切除术可降低血压水平，减少心血管发病率，降低肾素和醛固酮水平。在慢性心力衰竭中，醛固酮活性不适当升高，导致盐潴留；有人认为，由此导致的钙流失会导致继发性甲状旁腺功能亢进。随之而来的甲状旁腺激素引起的细胞内钙超载和氧化应激，以及相对醛固酮过多引起的放大作用，可能会增加心血管事件的风险。在原发性醛固酮增多症中，肾脏和粪便钙流失会触发 PTH 分泌增加，进而加重醛固酮分泌和心血管损害。这种序列解释了为什么肾上腺切除术和盐皮质激素受体阻断剂倾向于降低原发性醛固酮增多症患者的 PTH 水平。鉴于醛固酮和 PTH 之间的相互作用以及由此产生的潜在心血管损害，迫切需要研究评估针对这两种激素相互作用的诊断和治疗策略。
