The Acidifying Effect of Rubidium in Normal and Potassium-Deficient Alkalotic Rats 1

Abstract

Rubidium, element number 37, is an alkalimetal found in small quantities in the earth's crust, and in trace amounts in human tissues (1). Listed immediately below potassium in the Group I elements of the periodic table, rubidium possesses many of potassium's physical, chemical, and physiological properties. These two elements have qualitatively similar effects on the contraction of the isolated heart (2), on the depolarization of nerve or muscle preparations (3,4), and on the activity of certain intracellular enzyme systems (5, 6). The distribution of rubidium in human tissues resembles that of potassium (1, 7), and rubidium has been shown to be concentrated in certain plant cells (8) and in animal tissues (9, 10) with great rapidity. It has also been reported that addition of rubidium to a potassium-free diet will prevent the development in rats of most of the histological changes agsociated with potassium depletion (1).The central purpose of the present work was to compare the effects of rubidium aidd potassium ions on acid-base balance in normal and in potassium-depleted rats. When given an alkaline-ash, potassium-deficient diet, rats develop an alkalosis (12), which can be rapidly corrected by administration of potassium chloride (13)

Cation Accumulation by Muscle Tissue: The Displacement of Potassium by Rubidium and Cesium in the Living Animal12

“…They also confirm the previously reported fact that rubidium chloride lowers the blood CO2 content in alkalotic potassium-deficient rats (9) and extend the observations to demonstrate a similar, but less marked, acidifying effect of cesium chloride. Most significant of all, however, is the evidence presented here that despite very low plasma concentrations of these ions, muscle tissue may accumulate rubidium or cesium up to concentrations 20 to 60 per cent higher than that of potassium.…”

“…The foregoing observations confirm and extend the earlier data which had indicated that rubidium and cesium could be taken up in large quantities by muscle cells (6)(7)(8)(9). They also confirm the previously reported fact that rubidium chloride lowers the blood CO2 content in alkalotic potassium-deficient rats (9) and extend the observations to demonstrate a similar, but less marked, acidifying effect of cesium chloride.…”

“…2Presented in part at the Annual Meeting of the American Federation for Clinical Research, May, 1956. studies (6)(7)(8)(9) have already established in a general way that animal tissues are capable of accumulating significant quantities of rubidium or cesium, but there have been no determinations of the tissue-plasma concentration gradients when organisms are fed non-tracer amounts of these substances and no quantitative measurements of the extent to which these ions are taken up by tissues relative to potassium. The results of the present work indicate a distinctly greater affinity of rat muscle tissue for rubidium and cesium than for potassium, and the data therefore suggest that processes more complex than simple diffusion are involved in the normal accumulation of potassium.…”

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

“…Intracellular acidosis has been suggested as an explanation of the increased acid secretion of the potassium-depleted kidney (12)(13)(14). Conversely, it might also be suggested that in the rubidium-loaded animal intracellular pH is normal or increased, since accumulation of rubidium appears to be associated with the movement of acid out of cells (2,4). Renal tissue pH may fall only when the addition of a large exogenous acid load results in a net movement of acid back into cells.…”

“…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).…”