Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RUBIDIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources

Intracellular calcium and extra-retinal photoreception of Aplysia Giant neurons.

The early or "instantaneous" current-voltage relationship for the light-activated potassium current in Aplysia giant neurons was linear during the first second of illumination. However, the light current was greatly reduced or abolished by prolonged hyperpolarization. It was also greatly reduced by the injection of calcium EGTA buffers having calcium activities of 5.6 X 10(-8) M and simulated by injecting buffers with calcium activities of 2.8-5.6 X 10(-7) M. Removal of calcium from the extracellular fluid had no effect. Both the light- and calcium-activated outward potassium currents were reduced by tetraethylammonium (TEA) ions. The light current was not affected by substituting rubidium for potassium nor by substituting either lithium or Tris for sodium. The calcium-activated potassium current persisted when the neuron was cooled to 5 degrees C. However, the light response could no longer be elicited. Light hyperpolarizes Aplysia neurons probably by increasing intracellular calcium activity two-to six-fold which activates a membrane potassium conductance. Calcium levels appear to be restored within the cell and are energy dependent. The light-activated release of calcium is inhibited by cooling. The body wall of Aplysia transmits enough visible or 500 nm light to hyperpolarize some Aplysia giant neurons under ambient conditons. These neurons may be involved in the extraretinal light entrainment that occurs in Aplysia.

Animals↗

Effects of estrogens and progestogens on the membrane permeability and growth of human prostatic carcinoma cells (PC-3) in vitro.

The effects of estrogens and progestogens in the management of prostatic adenocarcinoma are generally believed to be related to their suppressive effect on the hypothalamic-pituitary-testicular axis, but other mechanisms have also been suggested. The present study was designed to investigate if an androgen-insensitive human prostatic cancer cell line (PC-3) is sensitive to estrogens or progestogens and to elucidate possible mechanisms of action. Both estrogens and progestogens in high doses (10(-5) M) suppressed tumor cell growth. At these high doses medroxyprogesterone acetate (MPA) most effectively reduced the uptake of 86rubidium chloride, indicating the strongest effect on ion transport and membrane permeability. Effects on rubidium transport were also seen after estrogen treatment. It is suggested that estrogens and progestogens have direct cytotoxic effects on prostatic carcinoma cells in vitro, possibly by an effect on the cell membrane.

Adenocarcinoma↗

The trehalose pathway and intracellular glucose phosphates as modulators of potassium transport and general cation homeostasis in yeast.

Trk, encoded by the partially redundant genes TRK1 and TRK2, is the major potassium transporter of Saccharomyces cerevisiae. This system is specific for potassium and rubidium but, by reducing the electrical membrane potential of the plasma membrane, Trk decreases the uptake of toxic cations such as lithium, calcium, aminoglycosides and polyamines, which are transported by other systems. Gain- and loss-of-function studies indicate that TPS1, a gene encoding trehalose-6-phosphate synthase and known to modulate glucose metabolism, activates Trk and reduces the sensitivity of yeast cells to many toxic cations. This effect is independent of known regulators of Trk, such as the Hal4 and Hal5 protein kinases and the protein phosphatase calcineurin. Mutants defective in isoform 2 of phosphoglucomutase (pgm2) and mutants defective in isoform 2 of hexokinase (hxk2) exhibit similar phenotypes of reduced Trk activity and increased sensitivity to toxic cations compared with tps1 mutants. In all cases Trk activity was positively correlated with levels of glucose phosphates (glc-1-P and glc-6-P). These results indicate that Tps1, like Pgm2 and Hxk2, increases the levels of glucose phosphates and suggest that these metabolites, directly or indirectly, activate Trk.

Adenosine Triphosphatases↗

Biochemical and morphologic characterization of acrylamide peripheral neuropathy.

To determine whether reduced Na+/K+-ATPase activity might be involved in acrylamide (ACR)-induced peripheral axon swelling and degeneration, rubidium (Rb+) transport was measured as an index of enzyme function. x-ray microanalysis was used to quantify elemental Rb uptake and accumulation in internodal myelinated axons, mitochondria, Schwann cells, and myelin of rat tibial nerve cryosections. Results demonstrated impairment of Rb uptake in tibial axons from orally intoxicated (2.8 mM ACR for 34 days), moderately affected rats. In severely affected oral rats (49 days), complete inhibition of Rb transport and frank axon degeneration were evident. However, in moderate-to-severely affected rats exposed to ACR via ip injection (50 mg/kg/day for 11 days), neither structural nor enzymatic changes were present in tibial fibers. These findings in nerve cryosections suggested inhibition of axolemmal Na+ pump activity and degeneration were dependent upon route of ACR administration. This possibility was substantiated by a quantitative longitudinal morphometric study of conventionally fixed tibial nerve. Oral ACR treatment (2.8 mM ACR for 15-49 days) was associated with progressive axon degeneration, which was preceded by atrophy. Axonal swellings were rarely (<1%) observed. In contrast, ip ACR injection (50 mg/kg/day for 5-11 days) produced classic behavioral neurotoxicity but did not alter axon morphology in tibial nerve. Thus, fiber degeneration and decreased Na+ pump activity were consequences of subchronic oral ACR administration. This parallel expression suggests a mechanistic relationship. However, the corresponding general neurotoxicological significance is unclear since, behavioral toxicity induced by ip ACR develops without structural and enzymatic changes in tibial nerve.

Acrylamide↗

Blood perfusion of subcutaneous tumours in mice following the application of low-level direct electric current.

Electrotherapy with low-level direct electric current has been proved to be an effective local treatment of solid tumours. In the presented study an attempt was made to evaluate the effect of a single treatment with electrotherapy on blood perfusion of solid subcutaneous fibrosarcoma Sa-1 tumours in A/J mice. The tissue-staining method with Patent blue-violet dye, the rubidium extraction technique, and the noninvasive near-infrared spectroscopy method were used for this purpose. Results of all methods indicate that perfusion and subsequently oxygenation of tumours were reduced due to application of electrotherapy.

Animals↗

Membrane transport changes in an adriamycin-resistant murine leukemia cell line and in its sensitive parental cell line.

Multidrug resistance in cancer chemotherapy occurs when cells develop resistance towards structurally and functionally unrelated drugs. It is speculated that alteration of some fundamental process(es) in the cells leads to the development of multidrug resistance. The sodium pump activity of murine leukemia cell lines P388/S (sensitive) and P388/ADR (resistant) was measured and found to be different in the two cell lines. The rate of sodium pumping, i.e., the ouabain-sensitive rubidium uptake, was consistently lower in the resistant cells compared to their parental controls. Uptake of adriamycin was lower in the resistant cells. Depolarizing the cells with potassium chloride or by inhibiting the pump with ouabain increased the adriamycin uptake in the sensitive cells but not in the resistant cells. Adriamycin did not have any acute effects on the sodium pump activity. It is concluded that the development of drug resistance in cell line P388 is associated with a decrease in sodium pump activity and a lack of depolarization-induced adriamycin uptake; these processes may be causally linked via alterations in cytosolic calcium concentration.

Animals↗

A 23-pS Ca2(+)-activated K+ channel in MCF-7 human breast carcinoma cells: an apparent correlation of channel incidence with the rate of cell proliferation.

In studies on the apical membranes of cultured MCF-7 human breast carcinoma cells, we found two conspicuous K+ channel types with conductances of 23 and 70 pS, respectively. Of these, the 23-pS K+ channel was most conspicuous. In cell-attached patches with KCl in the pipette, it had a linear current/voltage (I/V) relation and was activated by depolarisation and in excised inside-out patches it was highly selective for K+ over Na+ (permeability ratio of Na+ to K+, PNa/PK = 0.02). Rubidium (Rb+) had a similar permeability to K+, although it was only conducted at 20% of the rate of K+, and cesium (Cs+) had a permeability less than 30% that of K+ and was not conducted at all. Both Cs+ and Rb+ acted as partial blockers when applied internally but the channel was not blocked by external tetraethylammonium (TEA, 10 mmol/l), quinidine (200 mumol 1) or apamin (50 nmol/l). It was activated by Ca2+ in the range 10(-7)-10(-6) mol/l. In cell-attached patches at a pipette potential of O mV, the open-time histogram was described by a single exponential (time constant 1.6 ms) and the closed-time histogram by two exponentials (time constants 0.5 and 1.5 ms). The incidence of the 23-pS but not the 70-pS channel depended on the rate of cell proliferation. Thus, in studies on cell-attached patches from cells in the exponential growth phase, the 23-pS channel was observed in 78% of patches.(ABSTRACT TRUNCATED AT 250 WORDS)

Apamin↗

Effects of cold exposure and hibernation on renal Na,K-ATPase of the jerboa Jaculus orientalis.

Changes in activity and abundance of renal Na,K-ATPase were evaluated during cold exposure and hibernation of the jerboa Jaculus orientalis by measuring the hydrolytic activity, the number of units and the transport activity of Na,K-ATPase in isolated nephron segments. As compared to controls, jerboas exposed to cold (6 degrees C) for 4-5 weeks displayed mild diuresis, decreased urinary osmolality and increased kaliuresis. In cold-exposed jerboas, Na,K-ATPase hydrolytic activity was reduced in the medullary thick ascending limb and enhanced in the cortical and outer medullary collecting duct, whereas it was not altered in other nephron segments. The number of Na,K-ATPase units and the activity of Na,K-pump, determined by [3H]-ouabain binding and by ouabain-sensitive rubidium uptake respectively, changed in parallel with the hydrolytic activity in the medullary thick ascending limb and cortical collecting duct. The maximal rate of activity (Vmax) of Na,K-ATPase was not modified further during hibernation. Thus, cold exposure, but not the onset of hibernation, induces segment-specific changes in the abundance and activity of Na,K-ATPase units which are likely to be related to the entry into hibernation, but not to the maintenance of some renal functions during deep hibernation.

Animals↗

Effect of lithium and other alkali metals on brain chemistry and behavior. II. Intracranial self-stimulation behavior.

Rats implanted with bipolar electrodes aimed at the medial forebrain bundle (MFB) were trained to self-stimulate. Six daily injections of 2 mEq/kg of the chloride salts of Li+, Rb+ or Cs+ were administered and the rate of intracranial self-stimulation (ICSS) was recorded. Lithium caused a reversible decrease in ICSS rate, beginning on the second day and returning to pretreatment rate on the fourth day of injections. The decrease was more pronounced in animals with high baseline rate (over 500 responses/10 min) than in low responders. Rubidium enhanced ICSS rate whereas cesium had no effect. These results agree with other accumulating data showing the opposite effects of Li+ and Rb+, but their relevance to effective disorders is not clear.

Affective Symptoms↗

Renal blood flow during ureteral obstruction measured with 133Xe wash out, 86Rb uptake techniques and with an electromagnetic flowmeter.

In moderate mannitol diuresis in the dog the ratio RBF-86Rb uptake/RBF-electromagnetic flowmeter decreased during ureteral obstruction from 0.923 - 0.705. In the same animals the ratio RBF-133Xe wash-out/RBF-electromagnetic flowmeter increased from 0.932 - 1.365. With the rubidium technique a significant redistribution of intrarenal blood flow was observed. No similar flow changes were seen with the 133Xe wash-out technique. The two methods do not measure during ureteral obstruction the true RBF. The change of 86Rb uptake by the individual segments of renal tissue is not an unequivocal proof for the intrarenal redistribution of blood flow, but this possibility cannot be definitely excluded.

Animals↗

Determination of cardiac output in the mouse.

A technique is described for determination of cardiac output in the mouse. The method is basically a tracer dilution technique using 86-rubidium as soluble indicator, where a microsampler is used for blood collection and in which the gamma function fitting is applied for area determination.

Animals↗

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. I. Effects of different medium potassium concentrations on electrical parameters.

When serosal medium potassium was decreased from the usual concentration of 3.5 mM, the short-circuit current (SCC) of hemibladders in chambers immediately and transiently increased. The maximum SCC attained was greater the greater the decrease in serosal potassium, and was twice the initial SCC when the final serosal medium was potassium-free. The SCC then fell to its previous level for final serosal potassium concentrations greater than 2 mM and to less than its previous level for those less than 2 mM, being lowest (15% of previous levle) in potassium-free sodium Ringer's. When serosal medium potassium was increased from 3.5 mM by substituting potassium for sodium, SCC transiently decreased and then recovered to its previous level. Steady SCC was the same in serosal media of 2-116 mM potassium; conductance increased and p.d. decreased after incubation in 50-116 mM potassium serosal media. Short-circuit current and p.d. transiently increased (decreased) whenever serosal medium potassium was decreased (increased); conductance increased with any change in serosal potassium. Changing mucosal medium potassium concentration between 0 and 50 mM did not affect SCC. The initial transient increase and subsequent decrease in SCC on removing serosal potassium were partially prevented by 3.5 mM rubidium or caesium, or by 116 mM choline in the serosal medium. The transient changes in SCC were due partly to changes in transepithelial sodium transport.

Animals↗

Stoichiometry and ion affinities of the Na-K-Cl cotransport system in the intestine of the winter flounder (Pseudopleuronectes americanus).

Na-K-Cl cotransport stoichiometry and affinities for Na, K and Cl were determined in flounder intestine. Measurement of simultaneous NaCl and RbCl influxes resulted in ratios of 2.2 for Cl/Na and 1.8 for Cl/Rb. The effect of Na and Rb on Rb influx showed first order kinetics with K1/2 values of 5 and 4.5 mM and Hill coefficients of 0.9 and 1.2, respectively. The effect of Cl on rubidium influx showed a sigmoidal relationship with K1/2 of 20 mM and a Hill coefficient of 2.0. The effects of variations in Na and Cl concentration on short-circuit current (Isc) were also determined. The K1/2 for Na was 7 mM with a Hill coefficient of 0.9 and the K1/2 for Cl was 46 mM with a Hill coefficient of 1.9. Based on the simultaneous influx measurements, a cotransport stoichiometry of 1Na:1K:2Cl is concluded. The Hill coefficients for Cl suggest a high degree of cooperativity between Cl binding sites. Measurements of the ratio of net Na and Cl transepithelial fluxes under short-circuit conditions (using a low Na Ringer solution to minimize the passive Na flux) indicate that the Cl/Na flux ratio is approximately 2:1. Therefore, Na recycling from serosa to mucosa does not significantly contribute to the Isc. Addition of serosal ouabain (100 microM) inhibited Rb influx, indicating that Na-K-Cl cotransport is inhibited by ouabain. This finding suggests that a feedback mechanism exists between the Na-K-ATPase on the basolateral membrane and the apical Na-K-2Cl cotransporter.

Animals↗

Serum stimulation of sodium transport in human fibroblasts containing low and high levels of intracellular sodium.

The relationships between intracellular sodium content, sodium transport and serum effects were investigated in human fibroblasts. In the cells with low intracellular sodium (Na+iL; 0.04 mumol sodium/mg protein), serum stimulated the sodium-potassium pump as measured by ouabain-sensitive sodium efflux and rubidium influx and also exerted a transstimulation of ouabain-insensitive sodium transport resulting in net influx. In cells with high intracellular sodium (Na+iH; 0.42 mumol sodium/mg protein) all aspects of sodium transport were increased compared to Na+iL cells. In these cells serum caused no change in sodium-potassium pump activity but significantly increased the ouabain-insensitive sodium fluxes resulting in net efflux. In Na+iL cells, serum promoted net sodium influx through an amiloride-sensitive pathway that was undetectable in the basal state. In Na+iH cells the serum-stimulated net efflux was amiloride sensitive but this pathway also contributed to a major portion of sodium transport in the basal state. This study demonstrated that sodium-potassium pump activity is directed by the supply of internal sodium and that serum can increase this supply by promoting net influx, and that serum-induced sodium transport can be modified by intracellular sodium content.

Animals↗

Potassium-39 NMR of K+ interaction with the gramicidin channel and NMR-derived conductance ratios for Na+, K+ and Rb+.

A potassium-39 NMR study of potassium ion interaction with the gramicidin transmembrane channel in phospholipid bilayers at high ion activity is reported which allows determination of a weak binding constant, Kwb approximately equal to 8.3/M, and an off-rate constant for the weak site, kwoff approximately equal to 2.6 X 10(7)/sec. These values are interpreted with the aid of additional NMR data as the binding constant for formation of the doubly occupied channel state and the rate constant for an ion leaving the doubly occupied state. Considering the singly occupied channel state for the potassium ion to be "electrically silent" at 1 molar ion activity, as with the sodium ion, the single-channel conductance for 100 mV and 30 degrees C calculated to be 29 pS, and using the same approximation with previous NMR results on the sodium and rubidium ions, reasonable conductance ratios were calculated. Further experimental estimates of the other three constants with the experimental location of binding sites and Eyring rate theory to introduce voltage dependence allowed a more complete calculation of the two-site channel. The single-channel conductance for potassium ion is calculated to be 24 pS at 1 M activity and 26 pS at 0.6 M activity, which compares for diphytanoyl phosphatidylcholine membranes to an experimental most probable single-channel conductance of 25 pS and a mean channel conductance of 20 pS. The calculated conductance ratios using NMR-derived constants were gamma (K)/gamma (Na) = 2.0 and gamma (Rb)/gamma (Na) = 4.3.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric Conductivity↗

Anion transport during maturation of erythroblastic cells.

Bromide uptake was measured in single maturing erythroblastic cells of rabbits by means of X-ray microanalysis. Increase in bromide uptake as the cells matured was observed. The order of cells from low to high bromide uptake was: early erythroblast less than late erythroblast less than marrow red cells less than peripheral red blood cells. The transition from low to high bromide uptake is correlated to the accumulation of iron which begins in the late erythroblast. A decrease in rubidium uptake also occurs as iron accumulates in the cell. These results indicate that the anion and cation transport changes during maturation are parallel in time course but opposite in direction. In addition, the increase in bromide uptake can be accounted for by the increase in surface-to-volume ratios of the cells. Surface-to-volume ratios were estimated by morphometric techniques.

Animals↗

Clinical cardiac PET using generator-produced Rb-82: a review.

Cardiac positron emission tomography (PET) with generator-produced rubidium-82 (Rb-82) provides information not previously available for optimal diagnosis and management of cardiac disease. This new information includes the accurate, noninvasive diagnosis of coronary artery disease in asymptomatic or symptomatic patients, the noninvasive assessment of coronary stenosis severity, myocardial infarct imaging, myocardial viability, collateral function, and cardiomyopathy. Cardiac positron imaging may be carried out economically at the same or less cost as other high-tech diagnostic imaging but provides perfusion and metabolic information quantitatively for routine clinical studies not available by other diagnostic modalities.

Coronary Disease↗

Effects of hyperoxia on biochemical indexes of pig aortic endothelial function.

To determine what biochemical indexes might be useful in measuring the endothelial response to hyperoxia in vitro we exposed endothelial cell monolayers (ECM) from pig aortas to either hyperoxic (95% O2:5% CO2, 1 atm) or control conditions (95% air:5% CO2) and made the following measurements: (a) DNA and protein contents remaining in the ECM; (b) lactate dehydrogenase (LDH) activity in the medium; (c) the net uptake of rubidium (Rb+), adenine, and adenosine; and (d) cellular ATP and medium lactate. Twelve hours of hyperoxic exposure did not cause significant changes. After 24 or 48 h of hyperoxia, DNA and protein contents were decreased; LDH activity and the protein-to-DNA ratio were increased; adenosine uptake was decreased per ECM but was unchanged when corrected for culture DNA and protein contents. Adenine uptake was unaltered as were cellular ATP content and medium lactate concentration. The net Rb+ uptake-to-DNA ratio was increased after 24 h but not after 48 h of hyperoxia. The extent of the DNA and LDH changes indicated that the cellular disturbance caused by hyperoxia was progressive from 12 to 48 h. Presence of superoxide dismutase (250 U/ml) prevented both the increase of LDH activity and the decrease of protein after 48 h but did not affect the decrease of DNA. These results suggest that the cells remaining in the ECM after hyperoxia have normal biochemical function and may represent a subpopulation of cells more resistant to oxygen toxicity than the damaged cells.

Adenine↗