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At least 19 recordsLinked to original sources
PubMed1970

Rubidium, sodium and ouabain interactions on the influx of rubidium in rat red blood cells.

1. The activation curve of rubidium influx by external rubidium in rat red cells showed an inflexion at a concentration around 0.2 mM. This inflexion point was displaced to the right by ouabain.2. The removal of sodium from the external solution changed the characteristics of the activation curve of rubidium influx. At external rubidium below 0.5 mM the uptake increased whereas above that concentration there was marked reduction. Thus the sodium-free effect on rubidium uptake is dependent on the external rubidium concentration.3. With 0.25 mM rubidium, the relationship between increase of rubidium influx and reduction of external sodium followed a more or less exponential function. All the increment was ouabain-sensitive.4. With a rubidium concentration above 0.5 mM the reduction of the rubidium uptake, as sodium was removed, followed curves of complex shape. With 10 mM rubidium, when sodium was reduced from 5 mM to zero, there was an increase instead of a further reduction. These results suggest interactions of several effects.5. The ouabain sensitivity of the rubidium influx in rat red cells is smaller than in other systems studied up to now. The dose-response curve was shifted to the right as the rubidium concentration increased and a plateau was obtained with rubidium only below 1 mM at 10(-5)M ouabain. When plotted as a percentage of the maximal inhibition the points fell into the theoretical curve following a simple one reactant/one site reaction.6. Ouabain inhibition seems to be a complex function of at least three variables: the concentration of the glycoside, the concentration of sodium and the concentration of rubidium. When sodium was absent, 10 muM rubidium was able to prevent, to a great extent, the inhibition produced by 10(-5) and 10(-4)M ouabain.

Animals↗
PubMed1977

Bioassay method for polyene antibiotics based on the measurement of rubidium efflux from rubidium-loaded yeast cells.

A bioassay method for the polyene antibiotics nystatin and amphotericin B is proposed based on the measurement of the efflux of rubidium ions from a rubidium-loaded yeast culture challenged with the antibiotics. For this purpose a major proportion of the intracellular K(+) ions in a Saccharomyces cerevisiae culture has been substituted by Rb(+) ions. The rubidium leakage is measured by atomic absorption spectrophotometry, and a straight-line, dose-response correlation has been obtained for both antibiotics.

Amphotericin B↗
PubMed1992

The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--1. Rubidium.

The administration of TCP (15 mg/kg, i.p.) to rats pretreated with either intraperitoneal RbCl (3 mmol/kg, twice daily for 5 days) or dietary RbCl (30 mmol/kg diet, for 14 days), resulted in the complete 5-HT behavioural syndrome. Pretreatment with p-chlorophenylalanine (i.p. 300 mg/kg x2) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.) prevented the occurrence of the 5-HT syndrome, produced by dietary RbCl plus TCP. Intraperitoneal administration of RbCl had no effect upon the 5-HT behavioural syndrome, produced by 8-OH-DPAT (0.5 mg/kg, s.c.) or 5-MeODMT (2 mg/kg, i.p.) but enhanced the 5-HT syndrome produced by quipazine (20 mg/kg, i.p.), DOI (8 mg/kg, s.c.), p-chloramphetamine (4 mg/kg, i.p.) or by TCP plus L-tryptophan (50 mg/kg, i.p.) in rats. Dietary administration of RbCl resulted in the enhancement of the 5-HT2-mediated head-twitches in the mouse and the attenuation of hypothermia in the mouse, induced by 8-OH-DPAT (0.5 mg/kg, s.c.). The accumulation of 5-HT (after inhibition of monoamine oxidase) and the rate of synthesis of 5-HT in the whole brain (minus cerebellum) were enhanced by dietary and intraperitoneal administration of RbCl, respectively. The effects of lithium and rubidium, respectively, on 5HT function in brain are compared.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Rubidium in female Culicoides variipennis sonorensis (Diptera: Ceratopogonidae) after engorgement on a rubidium-treated host.

A rabbit given an intraperitoneal injection of 500 mg/kg of rubidium chloride retained elevated blood levels of Rb+ for at least 30 d with no overt effects. All Culicoides variipennis sonorensis (Wirth & Jones) females that fed on the rabbit 1, 4, 7, and 14 d after injection were marked with Rb+ when engorged (day 1), and 95% were marked when gravid (day 3). At 7 d, 79% of flies were marked, and 16% exhibited elevated levels after 14 d. Eggs laid 3-4 d after feeding contained elevated Rb+ levels, and the rapid decline in Rb+ content in females was associated with metabolism of the blood meal and oviposition.

Animals↗
PubMed2004

Synthesis and characterization of a series of rubidium alkoxides and rubidium-titanium double alkoxides.

This report investigates the structural aspects of the products isolated from the reactions of a series of titanium alkoxides [[Ti(OR)4]n n = 2, OR = OCH2C(CH3)3 (ONep) (1); n = 1, OC6H3(CH3)2-2,6 (DMP) (2)] with rubidium alkoxides [[Rb(OR)]infinity where OR = (ONep) (3), (DMP) (4), and OC6H3(CH(CH3)2)2-2,6 (DIP) (5)]. The resultant double alkoxides were determined by single crystal X-ray diffraction to be [Rb(mu-ONep)4(py)Ti(ONep)]2 (6), [Rb(mu-DMP)Ti(DMP)4]infinity (7), and [Rb(mu-DMP)2(mu-ONep)2Ti(ONep)]infinity (8). Compound 1 is the previously reported dinculear species with trigonal bipyramidal Ti metal centers whereas compound 2 is a monomer with a tetrahedral Ti center. Suitable X-ray quality crystals of 3 were not isolated. Compounds 4 and 5 demonstrate extended polymeric networks with Rb coordination ranging from two to five utilizing terminal mu- and mu3-OR ligands and pi-interactions of neighboring OAr ligands. The double alkoxide 6 revealed a simple tetranuclear structure with mu-ONep acting as the bridge, terminal ONep ligands on the Ti, and one terminal py on the Rb. For 7 and 8, the pi-interaction facilitated the formation of extended polymeric systems. All complexes were further characterized by FT-IR and multinuclear NMR spectroscopy.

Journal Article↗
PubMed1980

Rubidium block and rubidium permeability of the inward rectifier of frog skeletal muscle fibres.

1. A three-electrode voltage clamp method was used to investigate the Rb block of inward rectification in frog sartorius muscle fibres. 2. In a solution containing 80 mM-K+, the potassium conductance increased with increasing hyperpolarization to 3.18 +/- 0.11 mS. cm-2 (n = 17) when (V - VK) was -150 mV. In the presence of Rb+, the conductance increased, fell and increased again with increasing hyperpolarization, i.e. the Rb block was first increased and then reduced by increasing hyperpolarization. Increasing [Rb]o increased the block at all voltages. 3. In a solution containing 80 mM-Rb+ (zero K+) inward currents were recorded when the membrane was hyperpolarized beyond about -60 mV. These currents, which were < 10% the amplitude of those in 80 mM-K solution, were blocked by tetraethylammonium ions. 4. Experiments were carried out in solutions either where both [K]o and [K]i were increased, or where [K]o only was increased. The form of the relation between K conductance and membrane potential appeared to depend on [K]o. The magnitude of the conductance appeared to depend on [K]o and on [K]i. 5. So far as the block by Rb+ is concerned, increasing [K]o appeared to enhance the release of Rb block under large hyperpolarizations. Increasing [K]o and [K]i reduced the Rb block at all membrane potentials. 6. The results of experiments in the presence of Rb+ and Cs+ suggest that these two ions do not compete with each other for a site at which they block inward rectification. Rather, over a range of membrane potentials from -25 to -65 mV, the presence of Cs+ enhances the Rb block and vice versa. 7. Single dissected muscle fibres (from semitendinosus) were used to measure sarcoplasmic resistivity in 80 mM-K solution and 160 mM-K (hyperosmotic) solution. The measured values were 163.2 +/- 11.7 omega x cm and 136.1 +/- 16.0 omega x cm, respectively (n = 7). 8. A semi-empirical model is presented, supposing that Rb interacts with a site in the membrane to produce its blocking effect, but is able to move on through into the sarcoplasm. Internal K+ is supposed to reduce the affinity of the site for Rb+; external K+ is able to enhance the moving on of Rb+ into the sarcoplasm. 9. The implications of our experiments for the nature of the permeability mechanism inward rectification are discussed.

Animals↗
PubMed1985

Evidence for the ordered release of rubidium ions occluded within the Na,K-ATPase of mammalian kidney.

When Na,K-ATPase containing occluded rubidium ions is exposed to orthophosphate, in the presence of magnesium ions, there is a rapid release of half or all of the occluded ions. This behaviour is observed irrespective of whether the occluded-rubidium form of the enzyme is generated by putting the unphosphorylated enzyme in a sodium-free medium containing rubidium ions, or by allowing rubidium ions to catalyse the hydrolysis of phosphoenzyme made by adding ATP to enzyme suspended in a medium containing sodium and magnesium ions. The release of occluded rubidium ions by orthophosphate requires the presence of magnesium, presumably because phosphorylation is necessary. Whether the addition of orthophosphate causes the rapid release of all or of half of the occluded rubidium depends on whether free rubidium (or potassium, thallium or (probably) caesium ions) are present in the medium at the time the orthophosphate is added. In the absence of free ions of these species, all of the occluded rubidium is released. In their presence (in adequate concentration), only half of the occluded rubidium is released. The relative effectiveness of the different potassium congeners in preventing the rapid release of 50% of the occluded rubidium when orthophosphate is added is: thallium greater than rubidium greater than potassium greater than caesium. Lithium and sodium are ineffective even at high concentrations, and sodium ions strongly antagonize the effect of free rubidium ions. In a sodium-free, Tris medium, the concentration of free rubidium ions necessary for a half-maximal effect is about 30 microM. In a medium containing 250 microM-free rubidium, the concentration of sodium necessary to reduce the effect of free rubidium by 50% is about 500 microM. These figures are compatible with the hypothesis that the free rubidium or other ions act at the potassium-loading sites at the extracellular face of the pump. By starting with enzyme occluding unlabelled rubidium, and using 86Rb-labelled free rubidium, it is possible to show that the free ions that prevent the rapid release of half of the occluded ions themselves become occluded. These experiments are significant in two ways. First, they provide direct evidence for the existence of a second route for the release of occluded rubidium (and therefore presumably of occluded potassium) ions. Secondly, they seem to require that the release of occluded ions by this route occurs in an ordered fashion.

Animals↗
PubMed1989

Studies on the mechanism of rubidium-induced kaliuresis.

Renal clearance and electron microprobe methods were used 1) to elucidate the effects of chronic rubidium administration on potassium transport and 2) to localize, by the use of amiloride in acute experiments, the tubule site of interaction between rubidium and potassium. Substitution of drinking water by a 50 mM rubidium chloride solution for 9 to 11 days led to significant hypokalemia (plasma potassium 2.5 +/- 0.1 mM; plasma potassium plus rubidium 3.3 +/- 0.1 mM). Compared to a control group (reduction of plasma potassium to 3.4 +/- 0.1 mM by short-term potassium depletion) with a fractional potassium excretion of 2.1 +/- 0.3%, rubidium-treated rats excreted potassium at a much higher rate of 14.6 +/- 3.0%. The potassium content of principal cells was, however, significantly lower in rubidium-treated than in potassium-deprived animals. Similar to experiments in which rubidium was given acutely (3 hours), chronic rubidium administration was associated with preferential accumulation of rubidium in all tubule cells relative to potassium. Rubidium clearances were uniformly below those of potassium. Amiloride abolished the difference between rubidium and potassium clearances and sharply reduced the excretion of both cations. In view of the known site of action of amiloride, this suggests a distal tubule site of rubidium action on potassium transport. Amiloride also reduced or abolished the preferential uptake of rubidium into all but intercalated tubule cells. Marked cell heterogeneity of rubidium accumulation into intercalated cells was observed: One subpopulation, with low cell chloride, retained rubidium more effectively than another subpopulation with high cell chloride.

Amiloride↗
PubMed1982

Occlusion of rubidium ions by the sodium-potassium pump: its implications for the mechanism of potassium transport.

1. The occlusion of rubidium ions by Na, K-ATPase has been investigated by suspending enzyme prepared from pig kidney outer medulla in media containing low concentrations of (86)Rb, forcing the suspensions rapidly through small columns of cation-exchange resin, and measuring the amounts of radioactivity emerging from the columns.2. When the suspension media contained 2 mM-ATP or ADP, or 15 mM-NaCl, the amounts of radioactivity emerging from the columns were greatly (and similarly) reduced, presumably because both nucleotides and sodium ions stabilized the enzyme in the E(1) form. (See p. 19 for definition of E(1) and E(2)). The extra radioactivity carried through the columns when nucleotides and sodium were absent was taken as a measure of the amount of rubidium occluded within the enzyme (in the E(2) form) when it emerged from the resin.3. By varying the flow rate, and therefore the time spent by the enzyme on the resin, and relating this to the amount of radioactivity emerging from the columns, we have been able to estimate the rate constant for the conformational change (E(2) --> E(1)) that allows the occluded rubidium ions to escape. At 20 degrees C, and in the absence of nucleotides, it is about 0.1 S(-1).4. The rate constant for rubidium release was the same in a sodium-containing as in a potassium-containing medium. The opposite effects of sodium and potassium ions on the poise of the equilibrium between the E(1) and the E(2) forms of the enzyme must, therefore, be due solely to opposite effects of these ions on the rate of conversion of E(1) to E(2).5. The rate constant for rubidium release was greatly increased by ATP and by ADP. Both nucleotides appeared to act at low-affinity sites and without phosphorylating the enzyme.6. Orthovanadate, in the presence of magnesium ions, stabilized the enzyme in the occluded-rubidium (E(2)Rb) form.7. Ouabain, in the presence of magnesium ions, prevented the occlusion of rubidium ions.8. We have measured the amount of rubidium occluded by the enzyme as a function of rubidium concentration, and estimate that at saturating rubidium concentrations about three rubidium ions can be occluded per phosphorylation site (or per ouabain-binding site).9. We have found that the occluded-rubidium form of the enzyme can also be formed by allowing rubidium ions to catalyse the hydrolysis of phosphoenzyme generated by the addition of ATP to enzyme suspended in a high-sodium medium.10. The properties of the occluded-rubidium form of the enzyme, and of the two routes that can lead to its formation, suggest that an analagous occluded-potassium form plays a central role in the transport of potassium ions through the sodium-potassium pump. This hypothesis is supported by a detailed consideration of the probable magnitudes of the rate constants of the individual reactions making up the two routes.

Adenosine Diphosphate↗
PubMed2000

Gating and flickery block differentially affected by rubidium in homomeric KCNQ1 and heteromeric KCNQ1/KCNE1 potassium channels.

The voltage-gated potassium channel KCNQ1 associates with the small KCNE1 subunit to form the cardiac IKs delayed rectifier potassium current and mutations in both genes can lead to the long QT syndrome. KCNQ1 can form functional homotetrameric channels, however with drastically different biophysical properties compared to heteromeric KCNQ1/KCNE1 channels. We analyzed gating and conductance of these channels expressed in Xenopus oocytes using the two-electrode voltage-clamp and the patch-clamp technique and high extracellular potassium (K) and rubidium (Rb) solutions. Inward tail currents of homomeric KCNQ1 channels are increased about threefold upon substitution of 100 mM potassium with 100 mM rubidium despite a smaller rubidium permeability, suggesting an effect of rubidium on gating. However, the kinetics of tail currents and the steady-state activation curve are only slightly changed in rubidium. Single-channel amplitude at negative voltages was estimated by nonstationary noise analysis, and it was found that rubidium has only a small effect on homomeric channels (1.2-fold increase) when measured at a 5-kHz bandwidth. The apparent single-channel conductance was decreased after filtering the data at lower cutoff frequencies indicative of a relatively fast "flickery/block" process. The relative conductance in rubidium compared to potassium increased at lower cutoff frequencies (about twofold at 10 Hz), suggesting that the main effect of rubidium is to decrease the probability of channel blockage leading to an increase of inward currents without large changes in gating properties. Macroscopic inward tail currents of heteromeric KCNQ1/KCNE1 channels in rubidium are reduced by about twofold and show a pronounced sigmoidal time course that develops with a delay similar to the inactivation process of homomeric KCNQ1, and is indicative of the presence of several open states. The single channel amplitude of heteromers is about twofold smaller in rubidium than in potassium at a bandwidth of 5 kHz. Filtering at lower cutoff frequencies reduces the apparent single-channel conductance, the ratio of the conductance in rubidium versus potassium is, however, independent of the cutoff frequency. Our results suggest the presence of a relatively rapid process (flicker) that can occur almost independently of the gating state. Occupancy by rubidium at negative voltages favors the flicker-open state and slows the flickering rate in homomeric channels, whereas rubidium does not affect the flickering in heteromeric channels. The effects of KCNE1 on the conduction properties are consistent with an interaction of KCNE1 in the outer vestibule of the channel.

Animals↗
PubMed1984

A method for the study of cation transport in vivo: effects of digoxin administration and of chronic renal failure on the disposition of an oral load of rubidium chloride.

In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations following an oral load of rubidium chloride. The changes in plasma rubidium concentration are related to the distribution of rubidium to all the body tissues and the changes in intra-erythrocytic rubidium concentrations provide an example of rubidium uptake by one particular tissue. In eight healthy volunteers pretreatment with a loading dose of digoxin (20 micrograms/kg) enhanced the rise in plasma rubidium concentrations and attenuated the rise in intra-erythrocytic rubidium concentrations after the oral load of rubidium chloride. Ten patients with chronic renal failure, compared with a well-matched control group, were found to have changes similar to, but more marked than, those caused by digoxin, i.e. a much greater rise in plasma rubidium concentrations and a much smaller rise in intra-erythrocytic rubidium concentrations, after the oral load of rubidium chloride. These findings are consistent with wide-spread reduction in Na+, K+-ATPase activity in subjects who have taken a loading dose of digoxin and patients with chronic renal failure. They are, therefore, consistent with the findings of previous studies in vitro and show that it is possible to demonstrate changes in cation transport in vivo.

Adult↗
PubMed1988

Renal excretion of rubidium and potassium: an electron microprobe and clearance study.

A combination of clearance and electron microprobe studies was carried out to investigate renal rubidium excretion and rubidium distribution between plasma and individual tubule cells. Saline-infused animals were compared with potassium-loaded rats and another group in which rubidium was given in such amounts that the sum of plasma rubidium plus potassium equalled the potassium concentration in the potassium-loaded rats. The renal clearance of rubidium was uniformly less than that of potassium. Nevertheless, rubidium stimulated fractional potassium excretion above the levels observed in both saline- and potassium-loaded animals. When compared with their plasma concentrations, rubidium was concentrated in all tubule cell types more than potassium, and this is most likely due to restriction of passive diffusion of rubidium from cells to extracellular fluid. In addition, heterogeneity of intercalated cell ion composition was observed: one cell group had high chloride and potassium, but low rubidium contents, whereas the other was characterized by low chloride and potassium, but high rubidium contents.

Animals↗
PubMed1990

A non-invasive method of measuring concentrations of rubidium in rat skeletal muscle in vivo by 87Rb nuclear magnetic resonance spectroscopy: implications for the measurement of cation transport activity in vivo.

1. We have used n.m.r. spectroscopy to measure rubidium concentrations in the skeletal muscle of live intact rats. Using a 1.9 T superconducting magnet and an ear-phone coil tuned to both protons (1H) and rubidium (87Rb), it was possible to make measurements of both tissue rubidium content and water content, and from these measurements to obtain the rubidium concentration. 2. The n.m.r. estimate of rubidium concentration in muscle in vivo was found to be a constant 31% (SEM 4%) of that estimated by flame atomic absorption spectroscopy in an extract of excised muscle. This is close to the predicted theoretical n.m.r. visibility of 33%. The visibility was constant for muscle rubidium concentrations ranging between 10 and 34 mmol/l. 3. Rubidium concentration measurement by this method is unaffected by variations in sample geometry, sample volume, tissue conductivity, coil tuning and amplifier gain. 4. By using this method to measure changes in tissue rubidium concentration with time in the same animal, it should now be possible to assess the activity of ion transport systems, such as sodium- and potassium-activated adenosine triphosphatase in vivo, by measuring the rates of change of tissue rubidium concentrations during the administration of rubidium salts. 5. This method could also be used to measure the absolute concentration of any n.m.r.-visible nucleus and could be applied to man.

Animals↗