Romero J C, Knox F G, Opgenorth T J, Granger J P, Keiser J A
Fed Proc. 1985 May;44(8):2382-7.
The administration of aldosterone to normal subjects induces sodium retention, which is only transient inasmuch as sodium balance is restored shortly after extracellular fluid volume is expanded. This escape from sodium-retaining effects of mineralocorticoids, which is normally attended by sympathetic withdrawal, is not seen in some forms of secondary hyperaldosteronism that evolve with edema and increased sympathetic activity. The precise significance of the reflexly mediated changes in sympathetic activity on renal function has been difficult to assess. In fact, changes in cardiovascular volumes are known to be accompanied by alterations in other parameters that play a crucial role on salt and water equilibrium, such as renal perfusion pressure and renal renin. In this short paper we have analyzed the most probable integrated sequence of responses in neural activity, systemic pressure, and renal renin that lead to escape from high circulating levels of aldosterone. A major role is ascribed to volume expansion and to arterial pressure-induced natriuresis in the restoration of sodium balance. However, such responses are greatly facilitated by a selective inhibition of renal sympathetic activity mediated by cardiopulmonary receptors, and by a fall in postglomerular vascular resistance specifically mediated by a decrease in intrarenal angiotensin. These two modulatory factors are thought to assume a greater influence on sodium excretion during instances of secondary hyperaldosteronism.
给正常受试者注射醛固酮会导致钠潴留，但这种潴留只是短暂的，因为在细胞外液量增加后不久钠平衡就会恢复。这种对盐皮质激素钠潴留作用的逃逸现象，通常伴随着交感神经活动的减弱，在某些伴有水肿和交感神经活动增强的继发性醛固酮增多症中却看不到。交感神经活动反射性介导的变化对肾功能的确切意义一直难以评估。事实上，已知心血管容量的变化会伴随着其他对盐和水平衡起关键作用的参数的改变，如肾灌注压和肾素。在这篇短文中，我们分析了神经活动、全身压力和肾素中最可能的综合反应序列，这些反应序列导致从高循环水平的醛固酮中逃逸。在钠平衡的恢复中，容量扩张和动脉压诱导的利钠作用被认为起主要作用。然而，通过心肺受体介导的肾交感神经活动的选择性抑制，以及通过肾内血管紧张素减少特异性介导的肾小球后血管阻力的下降，这些反应得到了极大的促进。这两种调节因素被认为在继发性醛固酮增多症时对钠排泄有更大的影响。
