Intracellular Concentrations Of Na Research Articles

Sodium, potassium, and chloride fluxes in intercostal muscle from normal goats and goats with hereditary myotonia.

IN ISOLATED BUNDLES OF EXTERNAL INTERCOSTAL MUSCLE FROM NORMAL GOATS AND GOATS WITH HEREDITARY MYOTONIA THE FOLLOWING WERE DETERMINED: concentrations and unidirectional fluxes of Na(+), K(+), and Cl(-), extracellular volume, water content, fiber geometry, and core-conductor constants. No significant difference between the two groups of preparations was found with respect to distribution of fiber size, intracellular concentrations of Na(+) or Cl(-), fiber water, resting membrane potential, or overshoot of action potential. The intracellular Cl(-) concentration in both groups of preparations was 4 to 7 times that expected if Cl(-) were distributed passively between intracellular and extracellular water. The membrane permeability to K (P(K)) calculated from efflux data was (a) at 38 degrees C, 0.365 x 10(-6) cm sec(-1) for normal and 0.492 x 10(-6) for myotonic muscle, and (b) at 25 degrees C, 0.219 x 10(-6) for normal and 0.199 x 10(-6) for myotonic muscle. From Cl(-) washout curves of normal muscle usually only three exponential functions could be extracted, but in every experiment with myotonic muscle there was an additional, intermediate component. From these data PP(cl) could be calculated; it was 0.413 x 10(-6) cm sec(-1) for myotonic fibers and was 0.815 x 10(-6) cm sec(-1) for normal fibers. The resting membrane resistance of myotonic fibers was 4 to 6 times greater than that of normal fibers.

The exchange of radioactive cations by somatic and cardiac muscles of the crayfish

1. 1. Intracellular concentrations of Na +, K +, Ca 2+ and Mg 2+ were measured in a somatic muscle and in the heart of the crayfish. The uptake and the efflux of Na 24, K 42, Ca 45 and of Sr 89 were also measured. 2. 2. The initial influx rates of the ions from van Harreveld's solution into resting somatic muscle (in μEq/g cell water/hr) are: K + = 25; Na + = 56; Ca 2+ = 38. Similar figures were obtained for the heart muscle. 3. 3. The calculated permeability constants (× 10 8 cm/sec) are: P K = 64; P Na = 30 P Ca = 10; P Sr = 1·5. 4. 4. The stimulation of the muscle fiber leads to an additional Ca 2+ influx of about 2·8 pEq/cm 2 fiber surface. The additional Ca 2+ uptake is sufficient to account for the change in potential on the membrane. 5. 5. When muscles were immersed in Sr 2+ solutions, no additional Sr 89 uptake was found with stimulation. However, there is a high resting Sr 89 uptake and the muscle in Sr 2+ has a long refractory period, so a reasonable increase in Sr 89 uptake would not be detectable. 6. 6. The results are discussed in relation to the divalent cation mechanism for generating action potentials and to the part played by Ca 2+ in triggering contraction.

SODIUM-POTASSIUM-ACTIVATED ADENOSINE TRIPHOSPHATASE IN SCHIZOPHRENIC ERYTHROCYTES.

SINCE Skou's1,2 description of a sodium–potassium-activated adenosine triphosphatase in crab nerve, many reports have indicated that this enzyme has properties virtually identical to those exhibited by the Na+ extrusion mechanism in many tissues3–8. The intracellular concentrations of Na+ and K+ ions are of importance in regulating cell membrane excitability in nerve, muscle9, secretory cells, etc. It is also known10 that the amount of this enzyme in sheep erythrocyte membranes correlates with the intracellular concentration ratio of K+/Na+, which is in turn regulated by a gene11.

Effect of chlorothiazide on renal juxtaglomerular cells and tissue electrolytes.

Administration of chlorothiazide to rats for 9 weeks produces an increase of intracellular sodium and a decrease of intracellular potassium in skeletal muscle. However, in cardiac muscle, in the wall of mesenteric arterioles, in aortic wall, and in kidney there is no significant alteration in the amount of sodium, potassium, or chloride per unit of dry tissue weight. The water content of heart muscle, skeletal muscle, and kidney is not altered by chlorothiazide. The intracellular concentration of Na and K in heart muscle is likewise unaltered by chlorothiazide. However, chlorothiazide produces a highly significant 44% increase in the granularity of the juxtaglomerular cells. The data in general suggest that chlorothiazide decreases the volume of extracellular fluid, but does not reduce the content of intracellular Na. Extracellular K is reduced as well as the K inside skeletal muscle fibers. However, the amount of K inside cardiac muscle fibers is unchanged by chlorothiazide.