Escape from the sodium-retaining effects of mineralocorticoids: role of ANF and intrarenal hormone systems.
Escape from the sodium-retaining effects of mineralocorticoids: role of ANF and intrarenal hormone systems.
复制标题
逃避盐皮质激素的钠潴留作用：ANF 和肾内激素系统的作用。
DOI：
10.1038/ki.1989.51
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发表时间：
1989
影响因子：
19.6
通讯作者：
Knox,FG
中科院分区：
文献类型：
--
作者：
Gonzalez-Campoy,JM;Romero,JC;Knox,FG
慢性暴露于内源性或外源性盐皮质激素过量导致以低钾血症、代谢性水肿、多饮、多尿和轻度动脉压升高为特征的综合征。与这些激素的作用机制所预期的相反，只有短暂的正钠平衡期（图1）。即使在恢复钠平衡后，细胞外液体积的扩张仍得以维持，如体重增加所证明的。然而，这种细胞外液量的升高并不显著，充血性心力衰竭不是该综合征的一部分[1]。
Chronic exposure to either endogenous or exogenous mineralocorticoid excess results in a syndrome characterized by hypokalemia, metabolic alkalosis, polydipsia, polyuria, and mild arterial pressure elevation. Contrary to what might be expected from the mechanism of action of these hormones, there is only a transient period of positive sodium balance (Fig. 1). The expansion of the extracellular fluid volume is maintained as evidenced by an increase in body weight even after sodium balance is restored. However, this elevation of the extracellular fluid volume is not striking, and congestive heart failure is not part of the syndrome [1].