Comparison of renal excretion of rubidium and potassium

Kunin, Arthur S.; Dearborn, Earl H.; Burrows, Belton A.; Relman, Arnold S.

doi:10.1152/ajplegacy.1959.197.6.1297

Cited by 24 publications

(8 citation statements)

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“…These latter experiments revealed immediate rises in plasma potassium as rubidium entered cells (5). Increased renal excretion of potassium was shown to be the result of the hyperkalemia, there being no evidence for any direct effect of rubidium on renal tubular handling of potassium (6). Thus it would appear likely that in the present experiments transient elevations of plasma potassium were responsible for the kaluresis but had been dissipated in the 16 hours elapsing between the last load of rubidium and the time of blood sampling.…”

Section: Discussionmentioning

confidence: 92%

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

Lambie¹,

Relman²,

Schwartz³

1959

J. Clin. Invest.

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Previous studies have shown that administration of rubidium to normal or potassium-depleted rats results in a) metabolic acidosis (1), and b) accumulation of rubidium in muscle tissue where it attains final concentrations considerably higher than that of potassium (2). Since it was found that rubidium was at least as effective as potassium in lowering the plasma CO2 content of potassium-deficient nephrectomized animals (1), it was suggested that administered rubidium, like potassium, probably exchanges with intracellular hydrogen. ' In view of these facts it was deemed of interest to obtain information about the simultaneous renal and tissue exchanges of electrolytes during loading with rubidium. Short term balance studies were therefore carried out on rats given 40 mEq. per Kg. of RbCl over two days, and the results compared with those in control animals given an equivalent amount of KC1.The data to be reported show that acute loading resulted in the rapid accumulation of very large amounts of rubidium in tissues with the smaller quantity of sodium. A severe metabolic acidosis developed which was unaccompanied by compensatory increase in the urinary excretion of acid, thus demonstrating a renal defect which perpetuates the acidosis. METHODSMale albino rats of the Sprague-Dawley strain, weighing approximately 300 Gm., were used in all experiments. Four day balance studies were carried out, a two day control period on a standard liquid diet being followed by a two day period during which RbCl or KCl was added to the food. The composition of the diet fed during the control period is shown in Table I, its caloric value being approximately 2.5 calories per ml. The diet was administered by means of a stomach tube in four equal feedings per day; 87 ml. of diet per Kg. of weight was given, this being the largest quantity which could be administered without producing severe diarrhea. After 48 hours on the control diet the rats were divided into two groups. Group I, which consisted of 10 rats, was given a supplement of KCl, 20 mEq. per Kg. per day for the next two days, in addition to the standard control diet. Group II, consisting of 11 rats, received the control diet plus 20 mEq. per Kg. per day of RbCl to which tracer quantities of RbTM had been added. Thus the total load of rubidium or potassium for the two days of loading was 40 mEq.per Kg., an amount approximating the total quantity of potassium in the body. Tap water ad libitum was provided for drinking purposes throughout the experiment.To facilitate complete separation of urine and feces the animals were immobilized in light plaster casts. A modification of the cast described by Lathrop and Harper (4) was used, the chamber for the collection of expired gases being omitted from the design. The animals in TABLE I

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Section: Discussionmentioning

confidence: 92%

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

Lambie¹,

Relman²,

Schwartz³

1959

J. Clin. Invest.

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“…It appears that Rb is less mobile than K in the kidneys, since values of Q( Rb/K)( t ) for the kidneys increase from less than 1 soon after injection to about 3 at 45 min and settle near 1.6 within a few hours (Strauss et al 1975;Love et al 1954;Kilpatrick et al 1956;Mraz and Patrick 1957). We estimate from studies comparing uptake or clearance of Rb and K by the kidneys of mice, rats, rabbits and dogs (Strauss et al 1975;Moreno and Diamond 1974;Greger 1981;Kunin et al 1959;Kilpatrick et al 1956;Mraz and Patrick 1957) that Rb is taken up by kidney cells from the lumen and peritubular capillaries at rates about 0.55-0.95 times those of K. We have assigned an Rb extraction fraction for the kidneys of 0.85 because it is in the range of values observed by Mullani et al (1986) but slightly less than the value used earlier for K. This yields an inflow rate from plasma of 240 d-' (0.85 times a plasma flow of 0.19 X 1500 plasma volumes d-') and an outflow rate to plasma of 120 d-' (the total inflow as a fraction of total-body Rb is 0.003 times 240 d-' or 0.72 d-' , and since the kidneys contain 0.006 of total-body Rb, the outflow rate must be 0.72 d-'/0.006 or 120 d-I).…”

Section: Kidneysmentioning

confidence: 99%

“…Fast muscle fibers are more permeable to K via passive transport and probably receive little K by active transport. The greater values of Q( Rb/K) for slow muscle would then result from the more favorable competition of Rb with K during active transport than during passive transport (Kernan 1969;Kernan 1972;Kernan and McDermott 1973;Kunin et al 1959).…”

Section: Muscle (Skeletal)mentioning

confidence: 99%

A Biokinetic Model for Rb in Humans

Rw¹,

Lr²

1988

Health Physics

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Although whole-body retention of Rb in humans has been characterized reasonably well, current biokinetic models for Rb do not provide detailed or accurate descriptions of the time-dependent distribution of this element within the body. In this paper we construct a physiologically descriptive biokinetic model that closely tracks the movement of Rb from the time of intake until virtually all of the ingested or injected quantity has been removed from the body. The selection process for model parameter values is described for a reference adult male, but we demonstrate how the model may be applied to non-reference humans, including young children. It is shown that the model accurately predicts long-term retention of Rb in both sexes and in different age groups and depicts changes with time in the internal distribution of Rb with sufficient accuracy to be suitable for dosimetric estimates even for the short-lived isotope 82Rb (T 1/2 = 75 s).

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“…Ru bidium administered exogenously is reportedly distributed in various tissues including the brain (7-9) and is excreted very slowly (10,11). Repeated administrations of rubidium in certain doses, therefore, result in exhibiting toxic effects such as a decrease in body weight (8,12) and tetanic spasms or convulsion (12)(13)(14)(15).…”

Section: Discussionmentioning

confidence: 99%

Effects of Rubidium on Behavioral Responses to Methamphetamine and Tetrabenazine

Furukawa

Tokuda

1976

Japanese Journal of Pharmacology

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Abstract-Different groups of mice were injected subcutaneoLisly every other day with rubidium chloride at three doses (0.41(50), 1.23(150) and 3.69(450) meq,'kg (mg/kg)) or with saline as a control for a period of 2-3 weeks. Rubidium administered acutely did not affect spontaneous locomotor activities, while it tended to increase the activities when administered repeatedly though the increase was not statistically significant. The methamphetamine-induced hyperlocomotor activities were potentiated in the rubidium groups as compared with those in the saline group, this effect of rubidium being in creased with prolongation of repeated administrations. Monotonic decreases in ambu lation after tetrabenazine were not significantly affected in the rubidium-treated animals though the decreases were sometimes preceded by slight increases and recovery from the decrement tended to be more rapid. After tetrabenazine in the rubidium-treated groups, incidences of catalepsy were increased and jumping behavior and Straub tail responses occurred in a few cases. The results suggest that rubidium potentiates the excitatory action of methamphetamine on spontaneous locomotor activities, as con trasted with inhibitory influence of lithium.Rubidium and lithium, alkaline metals, have been proposed to have valuable therapeutic and prophylactic effects in manic-depressive psychosis; rubidium is principally effective in depressive states (1, 2) while lithium is effective mainly for manic states. In studies on ani mals, the behavioral activation caused by morphine is potentiated by rubidium in mice whereas it is antagonized by lithium (3). Thus rubidium and lithium presumably have opposite effects in all species.Many studies have also been done on the neurochemical mechanisms underlying the affective disorders. The catecholamine hypothesis of affective disorders is that some, if not all, depressions are associated with an absolute or relative decrease in catecholamines, available at central adrenergic receptors sites, while elation, conversely, may be associated with an excess of such amines (4, 5). Associated with this hypothesis has been the proposal by one of the present authors (T.F.) that lithium modifies behavioral responses to me thamphetamine and tetrabenazine and that these drugs act on the metabolism of endogenous brain catecholamines, inhibiting in particular the methamphetamine-induced excitation (6).The present investigation was an attempt to study the effects of rubidium on behavioral responses induced by methamphetamine and tetrabenazine. MATERIALS AND METHODSHealthy ddY male albino mice obtained from the Kuroda Animal Laboratory (Kuma

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Comparison of renal excretion of rubidium and potassium

Cited by 24 publications

References 0 publications

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

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

A Biokinetic Model for Rb in Humans

Effects of Rubidium on Behavioral Responses to Methamphetamine and Tetrabenazine

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