Disease relevance of rubidium

• Kinetics of rubidium-82 after coronary occlusion and reperfusion. Assessment of patency and viability in open-chested dogs [1].
• Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography [2].
• ICA-17043 blocked Ca(2+)-induced rubidium flux from human RBCs with an IC(50) value of 11 +/- 2 nM (CLT IC(50) = 100 +/- 12 nM) and inhibited RBC dehydration with an IC(50) of 30 +/- 20 nM [3].
• Unidirectional blood-to-brain and blood-to-tumor transport rate constants for rubidium 82 were determined using dynamic positron emission tomography in patients with primary or metastatic brain tumors [4].
• Accumulation of lipid-soluble ions and of rubidium as indicators of the electrical potential in membrane vesicles of Escherichia coli [5].

Psychiatry related information on rubidium

• Electrolyte metabolism in patients with periodic affective disorders during treatment with rubidium [6].
• 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 [7].
• Patients with alcohol abuse had diminished values of rubidium in nearly all analysed samples of cerebral nuclei (greater than 30% compared to normals), whereas the Rb values were normal or diminished in cortical regions [8].
• Alcohol consumption in rats treated with lithium carbonate or rubidium chloride [9].
• METHODS: Twelve patients with documented CAD and ischemic ST-segment depression during exercise testing were randomized to exercise training (n = 7) or sedentary life style (control; n = 5) and underwent rubidium-82 positron emission tomography pre- and postintervention [10].

High impact information on rubidium

• Finally, nitroprusside, thought to generate NO in vascular smooth muscle, relaxes rat aorta without increasing rubidium efflux [11].
• The activity of Na+, K+-activated adenosinetriphosphatase and the uptake of a potassium analog, rubidium, were found to be similar in cerebral microvessels and choroid plexus when measured in vitro [12].
• Regional [11C]HED retention was compared to regional blood flow as assessed by rubidium-82 [13].
• Agonist occupancy of the cloned human serotonin (5-HT)1A receptor expressed in HeLa cells stimulates Na+/K+ ATPase activity as assessed by rubidium uptake [14].
• When coexpressed in Xenopus oocytes with a beta subunit isolated from the same cDNA library, the ATPase is able to transport rubidium (a potassium surrogate) inward, and hydrogen outward, leading to alkalization of the intracellular compartment and acidification of the external medium [15].

Chemical compound and disease context of rubidium

• Oncogenic transformation of chick-embryo fibroblasts by Rous sarcoma virus alters rubidium uptake and ouabain binding [16].
• Nicotine elicited membrane depolarization, elevation of intracellular calcium, rubidium efflux, and release of insulin from mouse beta-TC6 insulinoma cells [17].
• The effect of captopril on renal blood flow in renal artery stenosis assessed by positron tomography with rubidium-82 [18].
• 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) [19].
• The relative contributions of Na(+)-K(+)-ATPase pumps and Na(+)-K(+)-Cl- cotransport to total rubidium (Rb+) influx into primary cultures of renal tubule cells (PC.RC) and cells transformed either with the wild-type or a temperature-sensitive mutant of the simian virus 40 (SV40), were measured under various growth conditions [20].

Biological context of rubidium

• Characterization of a new clone of ouabain-resistant CV1 cells (called OR8 cells) revealed a 5-fold increase in the IC50 for ouabain inhibition of rubidium uptake and a 10-fold increase in cell survival on ouabain [21].
• Noninvasive assessment of coronary stenoses by myocardial perfusion imaging during pharmacologic coronary vasodilation. VIII. Clinical feasibility of positron cardiac imaging without a cyclotron using generator-produced rubidium-82 [22].
• In this work we measure the time evolution of the population resulting from energy-transfer collisions as a function of the energy difference between the entrance and exit collisional channels using a sample of cold Rydberg atoms produced in a rubidium magneto-optical trap [23].
• Infarct size and viability imaged by PET using generator-produced rubidium-82 were quantified objectively by automated software and related to coronary arteriography, left ventricular ejection fraction, revascularization and 3-year mortality [24].
• Deuterium oxide intake normalized systolic blood pressure and aortic calcium uptake but not aortic rubidium 86 uptake in hypertensive rats on the high salt diet [25].

Anatomical context of rubidium

• Myocardial rubidium-82 tissue kinetics assessed by dynamic positron emission tomography as a marker of myocardial cell membrane integrity and viability [26].
• They also were shown to increase sodium influx and to decrease rubidium influx in monocyte preparations obtained from human blood [27].
• Liver cell recruitment (the equivalent of capillary recruitment in other organs) was explored by carrying out multiple indicator dilution experiments with labeled rubidium across the liver of the anesthetized dog under basal conditions and after bleeding with saline replacement infusion, which increases liver blood flow [28].
• Upon displacement of occluded rubidium, trypsin digests the Ca(2+)-bound and thermally inactivated 19-kDa membranes, and all of the membrane-embedded fragments are truncated or are split in these conditions [29].
• For both fibroblasts and adipocytes, the dependence of rubidium uptake activity on sodium concentration was characterized by K0.5 values of 9.4 and 6.2 mM, respectively, which is also diagnostic for the alpha 1 subunit in vivo [30].

Associations of rubidium with other chemical compounds

• Two functions of this enzyme were studied in adult, 1- and 6-week-old dogs and guinea pigs: in vitro myocardial uptake of rubidium (86Rb) and binding of ouabain [31].
• We have carried out a quantitative study of capsaicin-induced fluxes of sodium, guanidine, calcium, rubidium, and chloride ions in cultures of neonatal and adult rat DRG neurons, in conjunction with the use of a histochemical stain that identifies capsaicin-sensitive neurons by means of cobalt uptake [32].
• Up to 60 tissue samples were dissected from 13 human brains in defined regions and were analysed by means of neutron activation analysis for trace element concentration of cobalt, iron, rubidium, selesium, zinc, chromium, silver, cesium, antimony and scandium [33].
• As demonstrated by the patch clamp technique and rubidium (Rb+) efflux studies, neither mutation alters the properties of channel activities [34].
• Calcium ions have been shown to compete with two rubidium ions for occlusion sites on 19-kDa membranes, with a high affinity (KD approximately 2.8 microM, pH 7.5, 20 degrees C) [29].

Gene context of rubidium

• Tight coupling of rubidium conductance and inactivation in human KCNQ1 potassium channels [35].
• This can be explained by the observation that trk1 trk2 ppz1 or trk1 trk2 ppz1 ppz2 strains display a very poor rubidium uptake, with markedly increased Km values [36].
• 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 [37].
• We found that the entire Nha1p C-terminus domain is not necessary for either the proper localization of the antiporter in the plasma membrane or the transport of all four substrates (we identified rubidium as the fourth Nha1p substrate) [38].
• Treating cells with elevated extracellular potassium caused membrane depolarization and stimulation of rubidium efflux through KCNQ2 [39].

Analytical, diagnostic and therapeutic context of rubidium

• Regional myocardial perfusion and ischaemia were assessed by measurement of the uptake of rubidium-82 with positron tomography after mental arithmetic and physical exercise [40].
• Positron emission tomography (PET) centers without cyclotrons use generator-produced rubidium-82 (82Rb) for assessment of myocardial perfusion [41].
• The (Na+ + K+)-ATPase from 3T3-F442A fibroblasts and adipocytes was characterized by immunoblotting, ouabain-sensitive rubidium uptake, sodium affinity, and Northern analysis [30].
• In this report, a method is described to measure the fractional extraction of rubidium across the BBB using the constant intravenous infusion of rubidium-82 [42].
• The OLS immunoassay was validated against rubidium transport studies [43].

References