Watlington C, King R, Baldwin G, Grossman S, Estep H
Lancet. 1977 Jul 23;2(8030):169-71. doi: 10.1016/s0140-6736(77)90184-2.
Urinary extracts (in methylene dichloride) of subjects on high sodium-chloride (NaCl) intake produce net Cl- efflux (active transport) in isolated short-circuited frog skin. Activity is not found in the urine of NaCl-deprived normal subjects or NaCl-loaded subjects with adrenal insufficiency. These findings suggest that presence of an adrenocortical steriod which participates in adaptation to high salt intake. We describe here a lipid-soluble factor extracted from urine of chronically salt-loaded subjects which stimulates active Cl- transport in isolated frog skin. Our findings indicate that the factor is of adrenal origin and that it induces active ion transport in the direction opposite to that stimulated by the adrenal hormone, aldosterone. Aldosterone produces NaCl conservation in states of salt deprivation. We expect this new factor to produce NaCl excretion in states of excess salt ingestion.
高氯化钠（NaCl）摄入量受试者的尿液提取物（二氯甲烷溶液）可使离体短路蛙皮产生净氯离子外流（主动转运）。在缺钠的正常受试者或肾上腺功能不全的高钠负荷受试者的尿液中未发现该活性。这些发现表明存在一种参与高盐摄入适应过程的肾上腺皮质类固醇。我们在此描述一种从长期高盐负荷受试者尿液中提取的脂溶性因子，它可刺激离体蛙皮中的氯离子主动转运。我们的研究结果表明该因子源自肾上腺，且它诱导的主动离子转运方向与肾上腺激素醛固酮所刺激的方向相反。醛固酮在缺盐状态下可促进氯化钠的潴留。我们预计这种新因子在盐摄入过量状态下会促使氯化钠排泄。
