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PubMed1975

Rubidium redistribution after suprarenal caval ligation in the rat.

The distribution of infused 86 Rb Cl between different organs was followed for 48 hours. When SRVCL was perfused 15 hours after the 86 Rb Cl infusion, there was a redistribution with loss of Rb from the kidneys and the thigh musculature and an increase in the Rb concentration in the liver and shoulder musculature.

Animals↗
PubMed1995

Partial purification of a factor from the feline small intestine causing natriuresis in vivo and inhibiting rubidium uptake into renal cells in vitro.

Small intestine of cat was homogenized under denaturing condition (6.0 M guanidinium chloride) in the presence of protease inhibitors and molecules in the 500 to 10,000 Da mass range were obtained by sequential ultrafiltrations. This material was separated by gel chromatography (Sephadex G-25), where fractions eluted in the mass range of 500-1000 Da inhibited 86Rb uptake into kidney slices in vitro. Furthermore, the same fractions exhibited a natriuretic effect when given intravenously to anesthetized rats. The gel chromatography fractions were further purified by cation exchange chromatography (CM-Sephadex C-25). Fractions eluted with a NaCl solution of around 250 mM inhibited 86Rb uptake into renal cortical tissue in vitro and showed natriuretic activity when tested in vivo in rats. It is proposed that intestine contains a water soluble natriuretic factor with an apparent molecular mass of 500-1000 Da. This material evokes a natriuresis in vivo and inhibits 86Rb uptake in vitro.

Animals↗
PubMed1986

Interaction of monensin with dietary vanadium, potassium, and protein, and its effect on hepatic rubidium and potassium in chicks.

A series of experiments was undertaken to further investigate the influence of diet composition on chick response to monensin supplementation. Experiments were conducted to determine the effect of monensin on growth rate and hepatic Rb and K content as affected by dietary content of V, K, or protein. A factorial experiment involving V levels of 0, 5, 10, or 20 ppm and monensin levels of 0, 120, or 160 ppm was conducted with broiler chicks to 4 weeks of age. Growth rate was significantly depressed by 10 or 20 ppm V but not by monensin. Hepatic K content was not affected by dietary treatments. In another factorial experiment, effects of levels of 0 and 120 ppm monensin and 0 and 5 ppm V were compared. Growth rate was significantly depressed by both V and monensin but with no significant interaction. Neither hepatic Rb or K content was significantly altered by the supplements. A third factorial experiment involved monensin levels of 0, 120, or 160 ppm, added K levels of 0 or .3%, and dietary protein levels of 16 or 24%. Body weight at 3 weeks of age was significantly depressed by 160 ppm monensin in the high protein diet and by 120 or 160 ppm in the low protein diet. Added K did not counteract the growth depression. Hepatic Rb content was increased by monensin and significantly reduced by K supplementation. Hepatic K content was not increased by K supplementation. Chicks fed the low protein diet had significantly lower concentrations of hepatic Rb and K than those fed the high protein diet.

Animals↗
PubMed1984

Transport of calcium, germanium and rubidium ions in rice seedlings in deuterium oxide.

Deuterium oxide affected all types of transport processes of ions in rice seedlings. The processes of the active transport of Rb+, the passive diffusion of Ca2+, and the preferential and specific absorption of Ge by the seedlings in D2O solutions, were suppressively distorted by D2O. The suppressive effect on the translocation of all ions studied and the absorption of Rb+, was greater with higher concentrations of D2O. However, clear-cut relations of the effect of increasing D2O concentrations on the ion transport were not obtained. The extent of the replacement of H2O by D2O in the plant appeared to affect the movement of ions in the plant.

Biological Transport↗
PubMed1976

Effects of lithium and rubidium on antinociception and behaviour in mice. I. Studies on narcotic analgesics and antagonists.

The effects of acute and chronic LiCl and RbCl treatments on the antinociception caused by morphine, pethidine, methadone, pentazocine, nalorphine or naloxone were studied in mice using the hot plate and phenylquinone writhing tests. In both tests morphine, pethidine, and methadone caused significant antinociception whereas the antagonistic drugs were almost inactive. In the hot plate test both the 21 day administration of LiCl and the 5 and 21 day administration of RbCl decreased the antinociceptive effect of morphine. The 5 day administration of LiCl increased the antinociceptive effect of pethidine whereas the acute and 5 day administrations of RbCl abolished it. There were no significant or consistent interactions of the ions with the antinociceptive effect of methadone or the antagonistic drugs. In the phenylquinone writhing test the effects of the ions were inconsistent. Especially in the acute experiments where LiCl and RbCl had some effects on the behaviour of the mice treated with the analgesics, LiCl mostly impaired motor coordination and motor activity whereas RbCl was inactive or had opposite effects. LiCl enhanced the decrease in rectal temperature whereas RbCl was mostly inactive.

Analgesics, Opioid↗
PubMed1976

Effects of lithium and rubidium on antinociception and behaviour in mice. II. Studies on three tricyclic antidepressants and pimozide.

The effects of LiCl and RbCl on the antinociception caused by three antidepressants and pimozide were studied in mice. On the hot plate LiCl given acutely or chronically did not modify the antinociception of any drug although it augmented hypothermia induced by chlorimipramine and occasionally also that caused by desipramine and doxepine, and also caused definitive changes in motor abilities. RbCl given acutely (2.5 mEq/kg) or for 5 or 21 days in tap water (1 g/liter) abolished the antinociception caused by pimozide and when given acutely or for 5 days that of desipramine. In the phenylquinone writhing test LiCl when given for 21 days enhanced the nearly complete antinociception caused by chlorimipramine, doxepine and pimozide. These effects of ions did not seem to be related to changes in body temperature, motor coordination nor motility.

Animals↗
PubMed1975

Accumulation of lipid-soluble ions and of rubidium as indicators of the electrical potential in membrane vesicles of Escherichia coli.

We have studied the accumulation of dibenzyldimethyl-ammonium ion (DDA+) by respiring membrane vesicles of Escherichia coli, as an index of the generation of an electrical gradient during respiration. Nonrespiring vesicles accumulated DDA+ when K+ efflux was induced by valinomycin or monactin. By various criteria this was shown to be the exchange of one cation for another, independent of metabolism and coupled entirely by electrical forces. Uptake of DDA+ by respiring vesicles was inhibited by ionophores that translocate electrical charge and by reagents that block the respiratory chain. Oxamate and p-chloromercuribenzoate inhibited accumulation of DDA+ but did not dissipate a preformed pool; the reason appears to be that these reagents are less inhibitory to transport after lactate oxidation has begun than they are in resting vesicles. Uptake does not appear to involve a biological carrier, but requires trace amounts of a lipid-soluble anion such as tetraphenylboron, which has a catalytic role in DDA+ translocation. Respiring K+ vesicles accumulated substantially less DDA+ than did Na+ vesicles. Na+ was expelled from the vesicles concurrently with DDA+ uptake, whereas Rb+ and K+ were not. Thus, DDA+ uptake, whereas Rb+ and K+ were not. Thus, DDA+ uptake may be limited in the latter case by the availability of anionic groups. This explanation was supported by the finding that the addition of nigericin doubled the capacity of K+ vesicles to take up DDA+, presumably by providing a route for K+ to exit in exchange for H+. Parallel experiments on the valinomycin-dependent accumulation of Rb+ by respiring vesicles indicate that this process is analogous to the uptake of DDA+. Ionophores that elicit electrogenic K+ movement also induced respiration-linked transport. Proton-conducting ionophores and several inhibitors of respiration block Rb+ uptake and dissipated a preformed gradient. Preincubation of the vesicles with oxamate or p-chloromercuribenzoate inhibited Rb+ uptake, but their addition to respiring vesicles again did not cause efflux. Rb+ and DDA+ complete for uptake when present simultaneously. We conclude that the accumulation of both DDA+ and Rb+ occurs in response to an electrical gradient, vesicle interior negative, produced by respiration.

Antimetabolites↗