抄録
It is generally accepted that urine is concentrated by the mammalian kidney through the operation of a countercurrent mechanism in the renal medulla and that active sodium transport out of the ascending limb of Henle's loop plays an important role in this mechanism. In addition, it has been reported that in the adrenalectomized rat urine volume is decreased and the corticomedullary osmotic gradient lowered (1, 2).
Experiments studying the effects of aldosterone on free water clearance (3) and the attainment of maximum urinary osmolality (4), have suggested that aldosterone may cause an increased rate of transport of sodium from the inside of the ascending limb of Henle's loop to the surrounding tissue. On the other hand, the action of glucocorticoids, particularly their effects on the loop of Henle have not yet been precisely defined. Experiments dealing with free water reabsorption (TcH2O) indicated, that glucocorticoids may enhance sodium transport at the ascending limb (5, 6). Hierholzer's experiments (7) suggested that cortisol affects the water permeability of distal tubular segments. In the present experiments we have attempted, by microperfusion of Henle's loop in the kidneys of adrenalectomized rats, to clarify the mode of action of corticosteroids on these tubular segments.
