6533b7d0fe1ef96bd125abdb

RESEARCH PRODUCT

Die renale S�ure- und Ammonium-Ionen-Ausscheidung normaler und adrenalektomierter Ratten und ihre Beeinflussung durch Nebennierenrindenhormone

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The renal excretion of acid and ammonium ions after an oral load of monosodium-phosphate (1.2 mEq. per rat) was studied in groups of adrenalectomized er sham-operated rats, maintained on 0.9 per cent NaCI solution and water, on the 6th or 12th day after operation. Untreated groups were compared to groups receiving either Corticotropin (25 U./kg./day s.c.) or Cortisone acetate (12.5 mg./kg./day s.c.) er (7.5 mg./kg./day s.c.) or D,L-Aldosterone acetate Cortexone acetate (0.15 mg./kg./day s.c.) from the 3rd to the 12th day after opetarion. In sham-operated rats Cortisone increased H+ excretion and diuresis on the 6th day after operation (3rd day of treatment). This influence did not persist on the 12th day. Ammonium excretion also was enhanced by Cortisone and Aldosterone on the 6th day only, by Cortexone on the 6th and 12th day after operation. In adrenalectomized salt-maintained rats the renal excretion of H+ as weil of NH4 + ions after a phosphate load, was considerably depressed. The titratable acidity of the urine, though, was still higher than in adrenalectomized animals not given phosphate. The depression of H+ and 4 + excretion was counteracted by treatment with Cortisone and Cortexone, both hormones being more active on the 3rd than on the 9th day of treatment. Corticotropin or Aldosterone did not improve acid or ammonium excretion. It was concluded that suppression of adrenocortical secretion interferes with the renal tubular secretion of Hth and of NH4 + ions. While H+ secretion, though depressed, can still be raised by an acid load the excretion of NH4 + ions falls under the basic level. Disturbed renal ammonium excretion may, therefore, contribute to the development of metabolic acidosis in adrenalectomized salt-maintained rats .