Hemmung der extrarenalen Wirkung von d-Aldosteron durch Actinomycin D

Abstract

Experiments are described in which the distribution of sodium and potassium ions between the intra- und extracellular fluid of liver has been studied in nephrectomized adrenalectomized rats and in nephrectomized adrenalectomized rats given d-aldosterone (1 μg/150 g b.w., subcutaneously, single dose). d-Aldosterone has been found to decrease intracellular sodium concentration in liver and to increase the concentration quotient $$\frac{{{\text{Na}}^{\text{ + }} _e }}{{{\text{Na}}^{\text{ + }} _i }}$$ after a delay time of 90 min. Pretreatment with actinomycin D (300 μg/150 g b.w., i.p., single dose) prevents the aldosterone induced acceleration of cellular net sodium transport as well as the aldosterone induced increase in tubular sodium transport. Our findings indicate the aldosterone dependent increase in extrarenal cellular sodium transport being mediated by an induction of enzyme proteins as has been assumed by Edelman et al. as well as by Leaf et al. for the urinary bladder of Bufo marinus and the rat kidney. The results are discussed with respect to whether the enzyme system induced by aldosterone may function by increasing the permeability of the mucosal (luminal) cell membrane for sodium and a consequent increase in the availability of sodium to be transported through the serosal (peritubular) cell membrane, or by a channelling of metabolism to provide more energy for the active transport of sodium. It is difficult to apply the “permease” theory to explain the aldosterone dependent increase in hepatic cellular sodium transport resulting in a decrease in intracellular sodium concentration. Renal proximal transit time measured with lissamin green in adrenalectomized rats has been found to diminish with chronic treatment with d-aldosterone (1 μg/300 g b.w., s.c., daily for 4 days). This finding may explain why the effect of aldosterone decreases with chronic administration of the hormone. Although tubular reabsorptive capacity remains increased shortening of the contact of tubular fluid with the epithelial cells results in a reduction of the amount of sodium ions reabsorbed by the tubules under the influence of aldosterone.