Acid Excretion in Rubidium- And Cesium-Substituted Rats*†

Abstract

Previous studies have shown that rubidium or cesium can replace a major part of intracellular cation in vivo, and can correct the extracellular alkalosis associated with potassium depletion (1). In nephrectomized potassium-deficient animals it was demonstrated that rubidium, like potassium, lowers extracellular bicarbonate concentration by displacement of intracellular protons (2) [the latter perhaps transported out of cells by cationic amino acids (3)]. However, clear quantitative differences can be demonstrated between the effects of rubidium and potassium on extracellular bicarbonate: a) chronic administration of RbC1 to potassium-deficient alkalotic rats results in extracellular acidosis, whereas an equivalent amount of KCl merely restores extracellular bicarbonate concentration to normal (2); and b) acute loading of normal rats with RbCl produces a much greater reduction in extracellular bicarbonate than does an equivalent load of KCl (4).A remarkable feature of the extracellular acidosis produced in normal rats by acute loading with RbCl is the absence of any immediate renal compensation (4). Despite reduction of plasma CO2 content to 13 mMoles per L. there was no reduction in urine pH, and a slight fall, rather than an increase, in ammonium excretion. Since the administration of acid loads to rats ordinarily results in immediate and very large increments in acid excretion (5-7), the present study was undertaken to learn more about this apparently anomalous behavior of the rubidium-loaded kidney. Although loading with cesium does not produce significant extracellular acidosis, it was of interest to study the acid excretion of the cesium-substituted rat as well, and to compare both the cesium and rubidium preparations with the behavior of the normal and the potassium-depleted animal. METHODS AND MATERIALSMale white rats of the Sprague-Dawley strain weighing 200 to 400 Gm. were used in these studies. The animals were divided into four groups. The controls (Group I) consisted of 20 animals fed a low potassium diet for 17 days and then allowed to restore their deficits during a second 17 day period in which they received 20 mEq. per L. of KCI in their drinking water plus the basic diet. There were in addition 20 animals continuously fed on Purina® Chow and never depleted of potassium. Plasma electrolytes were the same in both these subgroups and their subsequent behavior in response to sodium chloride and ammonium chloride loads was indistinguishable. For the purpose of this study, therefore, the depleted-andthen-repleted animals were considered as normal and were grouped together with the Purina®D-fed animals, making a total of 40 animals in Group I. Group II consisted of 28 potassium-deficient animals studied immediately after 17 days on the potassium-free diet. Group III was composed of 26 rats which were fed the standard potassium-free diet for 17 days and then given RbCl, 20 mEq. per L., in their drinking water ad libitum for the next 17 days. The 30 animals in Group IV were similarly handled, but receiv...

Electrolyte and Acid-Base Balance During Acute Loading With Rubidium Chloride*†

“…There is good evidence in man and dog that loading with potassium inhibits secretion of acid (10), but the absence of any change in acid excretion in the potassium-loaded animals of this study, as well as other data in the literature (7,9), suggest that this phenomenon is not readily demonstrable in the rat. In any event, recent studies have shown that possible hydrogen-potassium competition cannot explain the behavior of rubidiumsubstituted rats, because there is no increased acid excretion even when urinary potassium and rubidium are very low (11). Further work will be required to clarify this question.…”

Renal function in sheep during infusion of alkali metal ions into the renal artery.

“…The ingestion of rubidium inhibits the renal excretion of acid thus preventing the metabolic alkalosis of potassium depletion and producing acidosis in both normal and potassium-depleted rats (Relman, Roy & Schwartz, 1953). To a lesser extent caesium ingestion also blocks the renal excretion of acid during potassium deficiency (Hall & Relman, 1959). In the dog the infusion of acidified lithium solutions suppressed the rate of hydrion secretion so that renal excretion of bicarbonate was increased (Orloff & Kennedy, 1952) and the infusion of isotonic lithium solutions produced concurrent increases in urine flow and in the renal excretion of sodium and potassium (Foulks, Mudge & Gilman, 1952).…”