Sodium-Induced Changes in the Nuclei of Monolayer Hela Cultures

1972 ◽  
Vol 11 (3) ◽  
pp. 669-673
Author(s):  
K. JOBST ◽  
N. KELLERMAYER
Keyword(s):  
Culture Medium ◽  
Structural Rearrangement ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Sodium Ions ◽  
Hypertonic Medium ◽  
Low Sodium ◽  
Large Numbers ◽  
Induced Changes ◽  
Cells Cultured

In HeLa cells cultured in a medium containing 142 mequiv./l. sodium ions only the mitotic forms are birefringent (anisotropic index, 27/1000). In a culture medium containing 155-160 mequiv./l. sodium ions, large numbers of nuclear forms reminiscent of the prophase were found. In such a medium the anisotropic index was 86/1000. At low sodium ion concentration (90-110 mequiv./l.) these anomalous, prophase-like forms were not seen and the anisotropic index was 18/1000. The appearance of the birefringent, prophase-like forms is related to a structural rearrangement and condensation of DNP in a hypertonic medium.

scholarly journals Identification of a Meningococcal l-Glutamate ABC Transporter Operon Essential for Growth in Low-Sodium Environments

2006 ◽  
Vol 74 (3) ◽  
pp. 1725-1740 ◽  
Author(s):  
Caterina Monaco ◽  
Adelfia Talà ◽  
Maria Rita Spinosa ◽  
Cinzia Progida ◽  
Eleanna De Nitto ◽  
...  
Keyword(s):  
Abc Transporter ◽  
Cell Invasion ◽  
Mutant Cell ◽  
Defined Medium ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Low Sodium ◽  
Defective Mutant ◽  
Secondary Transporter ◽  
Genes Encoding

ABSTRACT GdhR is a meningococcal transcriptional regulator that was previously shown to positively control the expression of gdhA, encoding the NADP-specific l-glutamate dehydrogenase (NADP-GDH), in response to the growth phase and/or to the carbon source. In this study we used reverse transcriptase-PCR-differential display (to identify additional GdhR-regulated genes. The results indicated that GdhR, in addition to NADP-GDH, controls the expression of a number of genes involved in glucose catabolism by the Entner-Doudoroff pathway and in l-glutamate import by an unknown ABC transport system. The genes encoding the putative periplasmic substrate-binding protein (NMB1963) and the permease (NMB1965) of the ABC transporter were genetically inactivated. Uptake experiments demonstrated an impairment of l-glutamate import in the NMB1965-defective mutant in the absence or in the presence of a low sodium ion concentration. In contrast, at a sodium ion concentration above 60 mM, the uptake defect disappeared, possibly because the activity of a sodium-driven secondary transporter became predominant. Indeed, the NMB1965-defective mutant was unable to grow at a low sodium ion concentration (<20 mM) in a chemically defined medium containing l-glutamate and four other amino acids that supported meningococcal growth, but it grew when the sodium ion concentration was raised to higher values (>60 mM). The same growth phenotype was observed in the NMB1963-defective mutant. Cell invasion and intracellular persistence assays and expression data during cell invasion provided evidence that the l-glutamate ABC transporter, tentatively named GltT, was critical for meningococcal adaptation in the low-sodium intracellular environment.

scholarly journals An Analysis of the Leakages of Sodium Ions into and Potassium Ions out of Striated Muscle Cells

1973 ◽  
Vol 61 (2) ◽  
pp. 222-250 ◽  
Author(s):  
R. A. Sjodin ◽  
L. A. Beaugé
Keyword(s):  
Steady State ◽  
Striated Muscle ◽  
Ringer Solution ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Sodium Ions ◽  
Sodium Influx ◽  
Potassium Efflux ◽  
Steady State Balance

Net sodium influx under K-free conditions was independent of the intracellular sodium ion concentration, [Na]i, and was increased by ouabain. Unidirectional sodium influx was the sum of a component independent of [Na]i and a component that increased linearly with increasing [Na]i. Net influx of sodium ions in K-free solutions varied with the external sodium ion concentration, [Na]o, and a steady-state balance of the sodium ion fluxes occurred at [Na]o = 40 mM. When solutions were K-free and contained 10-4 M ouabain, net sodium influx varied linearly with [Na]o and a steady state for the intracellular sodium was observed at [Na]o = 13 mM. The steady state observed in the presence of ouabain was the result of a pump-leak balance as the external sodium ion concentration with which the muscle sodium would be in equilibrium, under these conditions, was 0.11 mM. The rate constant for total potassium loss to K-free Ringer solution was independent of [Na]i but dependent on [Na]o. Replacing external NaCl with MgCl2 brought about reductions in net potassium efflux. Ouabain was without effect on net potassium efflux in K-free Ringer solution with [Na]o = 120 mM, but increased potassium efflux in a medium with NaCl replaced by MgCl2. When muscles were enriched with sodium ions, potassium efflux into K-free, Mg++-substituted Ringer solution fell to around 0.1 pmol/cm2·s and was increased 14-fold by addition of ouabain.

scholarly journals The Kinetics of Sodium Extrusion in Striated Muscle As Functions of the External Sodium and Potassium Ion Concentrations

1971 ◽  
Vol 57 (2) ◽  
pp. 164-187 ◽  
Author(s):  
R. A. Sjodin
Keyword(s):  
Sodium Ion ◽  
Ion Concentration ◽  
Potassium Ions ◽  
Sodium Ions ◽  
Sodium Efflux ◽  
Sodium Dependent ◽  
Na Efflux ◽  
External Potassium ◽  
Sodium Extrusion ◽  
Sodium And Potassium

After a 20 min initial washout, the rate of loss of radioactively labeled sodium ions from sodium-enriched muscle cells is sensitive to the external sodium and potassium ion concentrations. In the absence of external potassium ions, the presence of external sodium ions increases the sodium efflux. In the presence of external potassium ions, the presence of external sodium ions decreases the sodium efflux. In the absence of external potassium ions about one-third of the Na+ efflux that depends upon the external sodium ion concentration can be abolished by 10-5 M glycoside. The glycoside-insensitive but external sodium-dependent Na+ efflux is uninfluenced by external potassium ions. In the absence of both external sodium and potassium ions the sodium efflux is relatively insensitive to the presence of 10-5 M glycoside. The maximal external sodium-dependent sodium efflux in the absence of external potassium ions is about 20% of the magnitude of the maximal potassium-dependent sodium efflux. The magnitude of the glycoside-sensitive sodium efflux in K-free Ringer solution is less than 10% of that observed when sodium efflux is maximally activated by potassium ions. The inhibition of the potassium-activated sodium efflux by external sodium ions is of the competitive type. Reducing the external sodium ion concentration displaces the plots of sodium extrusion rate vs. [K]o to the left and upwards.

Effect of Ethanol, Diphenylhydantoin, Methotrexate and Low Sodium Ion Concentration on Jejunal Surface pH and Folic Acid Transfer in the Rat

1978 ◽  
Vol 6 (1) ◽  
pp. 297-299 ◽  
Author(s):  
MICHAEL L. LUCAS ◽  
SARA K. SWANSTON ◽  
FUNG HAN LEI ◽  
PAYUNG MANGKORNTHONG ◽  
JOHN A. BLAIR
Keyword(s):  
Folic Acid ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Surface Ph ◽  
Low Sodium

scholarly journals Restoration of the response of the middle cerebral artery of the rat to acidosis in hyposmotic hyponatremia by the opener of large-conductance calcium sensitive potassium channels (BKCa)

2017 ◽  
Vol 37 (9) ◽  
pp. 3219-3230 ◽  
Author(s):  
Marta Aleksandrowicz ◽  
Beata Dworakowska ◽  
Krzysztof Dolowy ◽  
Ewa Kozniewska
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Intracellular Signaling ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Sodium Ions ◽  
No Donor ◽  
Intracellular Signaling Pathway ◽  
Patch Clamp Electrophysiology ◽  
Channel Activator

Hyposmotic hyponatremia (the decrease of extracellular concentration of sodium ions from 145 to 121 mM and the decrease of hyposmolality from 300 to 250 mOsm/kg H2O) impairs response of the middle cerebral artery (MCA) to acetylcholine and NO donor (S-nitroso-N-acetyl-DL-penicillamine). Since acidosis activates a similar intracellular signaling pathway, the present study was designed to verify the hypothesis that the response of the MCA to acidosis is impaired during acute hyposmotic hyponatremia due to abnormal NO-related signal transduction in vascular smooth muscle cells. Studies performed on isolated, cannulated, and pressurized rat MCA revealed that hyposmotic hyponatremia impaired the response of the MCA to acidosis and this was associated with hyposmolality rather than with decreased sodium ion concentration. Response to acidosis was restored by the BKCa but not by the KATP channel activator. Patch-clamp electrophysiology performed on myocytes freshly isolated from MCAs, demonstrated that hyposmotic hyponatremia does not affect BKCa currents but decreases the voltage-dependency of the activation of the BKCa channels in the presence of a specific opener of these channels. Our study suggests that reduced sensitivity of BKCa channels in the MCA to agonists results in the lack of response of this artery to acidosis during acute hyposmotic hyponatremia.

Effects of sodium ion and solution tonicity on reactivities of hypertensive rat aortic strips

1960 ◽  
Vol 198 (5) ◽  
pp. 1019-1022 ◽  
Author(s):  
Samuel Mallov
Keyword(s):  
Drinking Water ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Nacl Solution ◽  
Hypertensive Rats ◽  
Initial Tension ◽  
Low Concentration ◽  
Ion Concentrations ◽  
Low Sodium ◽  
Hypertensive Rat

Rats were rendered hypertensive by injecting DCA and feeding 1% NaCl solution in place of drinking water. Isometric tensions developed by strips of aorta from these rats, when exposed to a low concentration of epinephrine, were compared with tensions developed by strips from normotensive controls, under conditions of varying Na ion concentration and solution tonicity. Solutions with high Na ion concentrations (hypertonic), and normal solutions rendered equivalently hypertonic by the addition of sucrose, increased the reactivities of strips from normotensive rats, but decreased the reactivities of strips from hypertensive rats, to added epinephrine. The hypertensive rat strips manifested increases in tension in these solutions even prior to the addition of epinephrine, so that the subsequent smaller responses to epinephrine may have been related to these initial tension increases. Low sodium ion concentrations in hypotonic solutions, but not in isotonic solutions, decreased the reactivities of both hypertensive and normotensive rat strips. These results are interpreted to mean that aortas from hypertensive rats are so changed structurally and functionally, that they respond differently than do normal aortas to increased sodium ion concentrations and/or hypertonic solutions, as well as to epinephrine in such solutions.

Residual phase lignin in haft cooking related to the conditions in the cook

1997 ◽  
Vol 12 (4) ◽  
pp. 225-229
Author(s):  
Cart-in A-S. Gustavsson ◽  
Chritofer T. Lindgren ◽  
Mikael E. Lindström
Keyword(s):  
Hydrogen Sulfide ◽  
Ionic Strength ◽  
Sodium Ion ◽  
Ion Concentration ◽  
Constant Composition ◽  
Hydroxide Ion ◽  
Sulfide Ion ◽  
Residual Phase ◽  
Kraft Cooking ◽  
Very High

Abstract The amount of lignin reacting according to the slow residual phase, i.e. the residual phase lignin, is in many perspectives an interesting issue. The purpose of the present investigation was to develop a mathematical model to show how the amount of residual phase lignin in the kraft cooking of spruce chips (Picm ahies) depends on the conditions in the earlier phases of the cook. The variables studied were hydroxide ion concentration, hydrogen sulfide ion concentration and ionic strength. The liquor-to-wood ratio during pulping was very high to maintain approximately constant chemical concentrations throughout each experiment (so called "constant composition" cooks). An increase in hydroxide ion concentration andtor hydrogen sulfide ion concentration leads to a decrease in the amount of residual phase lignin, while an increase in ionic strength, i.e. sodium ion concentration, leads to an increase. A signiticant result is that the hydrogen sulfide ion concentration has a pronounced influence on the amount of residual phase lignin during a cook at a low hydroxide ion concentration. The amount of residual phase lignin expressed as % lignin on wood, L,, can be described by the following equation developed for "constant composition" cooks (when cooking with a constant sodium ion concentration of 2 mol/L): LT=0,55-0.32*[HO-](-1,3)*ln[HS-] This equation is valid for a concentration of HO- in the range from 0.17 to 1.4, and a hydrogen sulfide ion concentration from 0.07 to 0.6 mol/L.

scholarly journals ALKALOSIS VERSUS ABNORMAL SODIUM ION CONCENTRATION AS A CAUSE OF TETANY

1923 ◽  
Vol 57 (1) ◽  
pp. 47-63
Author(s):  
W. Denis ◽  
L. von Meysenbug ◽  
Julia Goddard
Keyword(s):  
Sodium Ion ◽  
Ion Concentration
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