Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Boston, MA 02115, USA.
Hypertension. 2013 Apr;61(4):886-93. doi: 10.1161/HYPERTENSIONAHA.111.00662. Epub 2013 Feb 11.
Abnormal aldosterone physiology has been implicated in the pathogenesis of cardiometabolic diseases. Single aldosterone measurements capture only a limited range of aldosterone physiology. New methods of characterizing aldosterone physiology may provide a more comprehensive understanding of its relationship with cardiometabolic disease. We evaluated whether novel indices of aldosterone responses to dietary sodium modulation, the sodium-modulated aldosterone suppression-stimulation index (SASSI for serum and SAUSSI for urine), could predict cardiometabolic risk factors. We performed cross-sectional analyses on 539 subjects studied on liberal and restricted sodium diets with serum and urinary aldosterone measurements. SASSI and SAUSSI were calculated as the ratio of aldosterone on liberal (maximally suppressed aldosterone) to the aldosterone on restricted (stimulated aldosterone) diets and associated with risk factors using adjusted regression models. Cardiometabolic risk factors associated with either impaired suppression of aldosterone on liberal diet, or impaired stimulation on restricted diet, or both; in all of these individual cases, these risk factors associated with higher SASSI or SAUSSI. In the context of abnormalities that constitute the metabolic syndrome, there was a strong positive association between the number of metabolic syndrome components (0-4) and both SASSI and SAUSSI (P<0.0001) that was independent of known aldosterone secretagogues (angiotensin II, corticotropin, potassium). SASSI and SAUSSI exhibited a high sensitivity in detecting normal individuals with zero metabolic syndrome components (86% for SASSI and 83% for SAUSSI). Assessing the physiological range of aldosterone responses may provide greater insights into adrenal pathophysiology. Dysregulated aldosterone physiology may contribute to, or result from, early cardiometabolic abnormalities.
异常的醛固酮生理学与心脏代谢疾病的发病机制有关。单次醛固酮测量仅能捕捉到有限范围的醛固酮生理学。描述醛固酮生理学的新方法可能提供对其与心脏代谢疾病关系的更全面理解。我们评估了新的醛固酮对饮食钠调节的反应指标，即钠调节的醛固酮抑制-刺激指数（血清中的 SASSI 和尿液中的 SAUSSI），是否可以预测心脏代谢危险因素。我们对 539 名在低盐和高盐饮食下进行研究的受试者进行了横断面分析，并测量了血清和尿液中的醛固酮。SASSI 和 SAUSSI 分别表示在低盐（最大抑制的醛固酮）和高盐（刺激的醛固酮）饮食下的醛固酮比值，并使用调整后的回归模型将其与危险因素相关联。与低盐饮食下醛固酮抑制受损或高盐饮食下醛固酮刺激受损或两者兼有的心脏代谢危险因素相关；在构成代谢综合征的异常情况下，代谢综合征成分（0-4 个）的数量与 SASSI 和 SAUSSI 呈强烈正相关（P<0.0001），与已知的醛固酮刺激物（血管紧张素 II、促皮质素、钾）无关。SASSI 和 SAUSSI 在检测无代谢综合征成分的正常个体时具有很高的敏感性（SASSI 为 86%，SAUSSI 为 83%）。评估醛固酮反应的生理范围可能会提供对肾上腺病理生理学的更深入了解。失调的醛固酮生理学可能导致或源于早期的心脏代谢异常。
