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Results for “Sodium Isotopes”

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At least 37 records · Page 2Linked to original sources
PubMed1975

Inhibition of active sodium transport by radiographic contrast media.

We demonstrate that salts of diatrizoate and iothalamate, radiographic contrast agents, depress the active transport of sodium in the urinary bladder of the Columbian toad, Bufo marinus. Isolated toad bladders were incubated in isotonic Ringer's solutions with isosmolar displacement of sodium chloride by contrast media in experimental solutions. Sodium transport as measured both by short-circuit current (SCC) and by isotopic sodium flux was significantly depressed in the presence of sodium diatrizoate. Sodium transport measured by SCC was significantly depressed with sodium iothalamate and meglumine iothalamate. Equimolar methylsulfate Ringer's solution did not depress SCC. Although contrast media in isotonic Ringer's solutions depressed basal SCC, the vasopressin-stimulated increment in SCC was not depressed by contrast media. Separate experiments with hyperosmolar solutions (786 mM, as utilized in angiography) demonstrated equivalent suppression of SCC by contrast media and by other solutions made hyperosmolar with glucose or sodium methylsulfate, implying a general or nonspecific effect of hyperosomolarity. Inhibition of SCC by contrast media was reversible when the agents were removed by serial changes with standard Ringer's solution. Inhibition of sodium transport by contrast media might provide a basis for studies on some of the clinical toxicities of these agents.

Animals↗
PubMed1977

Inhibition of sodium transport by prostaglandin E2 across the isolated, perfused rabbit collecting tubule.

This study was designed to examine whether prostaglandin E2 can directly affect sodium transport across isolated perfused rabbit renal collecting tubules. Changes in transepithelial potential and isotopic sodium fluxes in response to peritubular prostaglandin E2 were measured. In addition, changes in transepithelial potential of the outer medullary collecting tubule in response to prostaglandin E2 were also measured. With few exceptions, all rabbits received 5 mg/day desoxycorticosterone acetate for 4-11 days before experimentation. The results of the experiments show that: (a) prostaglandin E2 inhibits the negative transepithelial potential in the cortical collecting tubule as well as the outer medullary collecting tubule; (b) prostaglandin E2 inhibits net sodium transport out of the lumen by inhibiting efflux while backflux is unaffected; (c) prostaglandin E2 produces this inhibition within 15 min, and the effects are dose dependent and reversible. These results suggest that prostaglandin E2 may modulate sodium transport in vivo and may contribute to the final regulation of sodium excretion.

Animals↗
PubMed1976

On the influence of the natriuretic factor from patients with chronic uremia on the bioelectric properties and sodium transport of the isolated mammalian collecting tubule.

A gel filtration fraction of urine from patients with chronic renal disease (natriuretic factor) has been shown previously to cause natriuresis in rats and to inhibit sodium transport in the isolated toad bladder. The effect of this fraction on transtubular potential difference and sodium transport was examined on the isolated perfused cortical collecting tubule of the rabbit. A rapid inhibition of potential difference from -22.5 mV to -12 mV (P less than 0.001) was observed when the fraction was applied to the peritubular surface. This effect was accompanied by a decrease in net sodium flux from 6.29 to 3.21 pmol/cm per s (P less than 0.001). Unidirectional fluxes using isotopic sodium revealed that the inhibition of net sodium transport was due to a decrease in flux from the lumen to the peritubular surface, i.e., an inhibition of active sodium transport. There was no change in sodium flux in the reverse direction. These changes were all rapidly reversed by removal of the fraction from the peritubular surface. The addition of the fraction to the lumen had no effect on potential difference or net sodium flux. Control studies using the same fraction from the urine of normal subjects had no effect on any of the parameters studies. Where both a uremic and a normal fraction were sequentially applied to the peritubular surface of the same tubule, inhibition of potential difference was obtained only with the former. In the light of evidence implicating the collecting duct fraction from normal animals, the data are consistent with the view that the natriuretic factor may be biologically important in the regulation of sodium balance via it's regulatory role in active sodium transport in the collecting tubule.

Animals↗
PubMed1987

Neurotoxin-modulated uptake of sodium by highly purified preparations of the electroplax tetrodotoxin-binding glycopeptide reconstituted into lipid vesicles.

Using the dialysable detergent CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate), the tetrodotoxin-binding protein from the electroplax of the electric eel has been purified to a high degree of both chemical homogeneity and toxin-binding activity. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the best preparations showed only a single microheterogeneous band at Mr approximately 260,000, despite attempts to visualize smaller bands by sample overloading. Upon dialysis, this material became incorporated into the membranes of small unilamellar vesicles, and in this form the purified protein exhibited tetrodotoxin-binding properties similar to the component in the original electroplax membrane. Furthermore, in the presence of activator neurotoxins the vesicles were able to accumulate isotopic sodium in a manner similar to that previously described for less active or less pure preparations of vesicles containing either mammalian or eel electroplax toxin-binding proteins. Quantitative consideration of the isotopic transport activity of this pure material, along with the high degree of purity of the protein, strongly suggests that the 260-kDa glycopeptide from electroplax is necessary and sufficient to account for the sodium channel function seen in these studies, and eliminates the possible involvement of smaller peptides in the channel phenomena observed.

Animals↗
PubMed2005

Human sulfate kinetics.

Electrospray tandem mass spectrometry was used to determine steady-state serum and urinary inorganic sulfate and sulfate ester kinetic profiles of nine normal men after intravenous injection of the stable isotope sodium [34S]sulfate. Sulfate ester appearance was traced by eliminating inorganic sulfate from samples, followed by hydrolysis of sulfate esters to inorganic sulfate for analysis. Whole body inorganic sulfate turnover in steady state was calculated using standard tracer techniques. Rate of appearance and disappearance of inorganic sulfate was 841 +/- 49 micromol/h. Average urinary inorganic sulfate excretion was 609 +/- 41 micromol/h, and the whole body sulfation rate (total rate of disappearance minus rate of urinary excretion) was 232 +/- 36 micromol/h. Tracer-labeled sulfate esters appeared in serum and urine within 1 h of tracer injection. The kinetics of inorganic sulfate and sulfate esters were linked by means of a compartmental model. The appearance and excretion of sulfate esters accounted for approximately 50% of the total sulfation rate. These results indicate that human whole body sulfation accounts for approximately 27% of inorganic sulfate turnover and that extracellular inorganic sulfate is an important pool for intracellular sulfation. A substantial fraction of newly synthesized sulfate esters promptly enters the extracellular space for excretion in the urine.

Fasting↗
PubMed1996

Quantitative tissue sodium concentration mapping of normal rat brain.

A quantitative in vivo method for obtaining maps of tissue sodium concentration (TSC) by MRI is compared to the invasive, global 22Na radionuclide dilutional technique in the normal rat brain. The MR method uses a three-dimensional projectional acquisition scheme to minimize signal losses from transverse relaxation. Internal calibration standards are used to convert the signal intensity into TSC after correction for B1 inhomogeneities by using the ratio of 23Na and 1H images obtained with identical B1 distributions and sensitivities at the two frequencies. Over the biological range of concentrations, the TSC, measured as the ratio of MR signals of 23Na and 1H, gives a linear response with concentration. In the normal rat brain, the mean TSC measured using the MRI method (TSC = 45 +/- 4 mM, animals = 5) is not significantly different from the global 22Na radionuclide method (TSC = 49 +/- 6 mM, animals = 7).

Animals↗
PubMed2002

The influence of water content on the 23Na and 31P NMR spectral parameters in solid Na-DNA.

23Na and 31P MAS NMR spectra and spin-lattice relaxation times in a solid sample of Na-DNA were measured under very carefully controlled conditions of relative ambient humidity. The observed substantial changes of the NMR parameters are related to the water-induced transitions between the different molecular configurations of DNA, with the transition between A- and B-DNA occurring in the 30-60% range of relative humidity. Our work demonstrates that the previously measured NMR parameters are in error because the relative humidity of the system had not been controlled, rendering the results irreproducible.

Animals↗