Der Einfluß eines Kaliummangels auf die renale Wirkung verschiedener Diuretica

Summary

Feeding rats a low potassium diet leads to a negative potassium balance of 1500 μeq/animal within two weeks.

Glomerular filtration has been found to be slightly reduced under this condition. Na⁺ and urea concentration gradients between the cortex and the tip of the papilla are markedly reduced. The antidiuretic action of vasopressin is diminished.

The results indicate that there is an impaired sodium transport in the ascending loop of Henle in addition to a decrease in water permeability likely to be explained by an increase in glucocorticoid secretion in potassium deficiency.

The sodium diuretic effect of chlorothiazide has been found reduced under the experimental conditions described. This finding may be explained by chlorothiazide mainly acting on the loop of Henle. With reduced sodium transport in this segment in potassium deficiency, a further decrease in sodium reabsorption caused by chlorothiazide will result in a smaller amount of sodium ions excreted than with a high rate of sodium transport in normal rats.

The sodium diuretic effect of furosemide has been found increased in potassium deficient rats. This result may be explained by furosemide acting on the proximal tubules and the ascending loop of Henle. Latter effect may partially prevent that there is a “corrective” reabsorption of sodium ions excluded from preceding proximal absorption under the influence of the drug. With decreased sodium transport in the loop of Henle, additional lowering of reabsorptive capacity caused by furosemide will result in a further decrease in the “correction” of the proximal effect.