Effects of low extracellular sodium concentration on reperfusion induced arrhythmias: changes in the myocardial sodium, potassium and calcium contents in isolated guinea pig hearts

1989 ◽  
Vol 23 (12) ◽  
pp. 993-1000 ◽  
Author(s):  
A. TOSAKI ◽  
M. KOLTAI ◽  
P. BRAQUET
1974 ◽  
Vol 52 (4) ◽  
pp. 898-901 ◽  
Author(s):  
D. Bose

Ouabain produced an increase in tension in the guinea-pig taenia coli which was abolished in the presence of high extracellular potassium. On the other hand the delayed inhibitory response of ouabain could only be abolished by the removal of extracellular sodium. The mechanism of inhibition of contraction by ouabain appears to be due to elevation of intracellular sodium concentration.


2021 ◽  
Vol 2021 (3) ◽  
Author(s):  
Jules Hancox

The sodium/calcium exchangers (NCX) use the extracellular sodium concentration to facilitate the extrusion of calcium out of the cell. Alongside the plasma membrane Ca2+-ATPase (PMCA) and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), as well as the sodium/potassium/calcium exchangers (NKCX, SLC24 family), NCX allow recovery of intracellular calcium back to basal levels after cellular stimulation. When intracellular sodium ion levels rise, for example, following depolarisation, these transporters can operate in the reverse direction to allow calcium influx and sodium efflux, as an electrogenic mechanism. Structural modelling suggests the presence of 9 TM segments, with a large intracellular loop between the fifth and sixth TM segments [1].


2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Jules Hancox

The sodium/calcium exchangers (NCX) use the extracellular sodium concentration to facilitate the extrusion of calcium out of the cell. Alongside the plasma membrane Ca2+-ATPase (PMCA) and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), as well as the sodium/potassium/calcium exchangers (NKCX, SLC24 family), NCX allow recovery of intracellular calcium back to basal levels after cellular stimulation. When intracellular sodium ion levels rise, for example, following depolarisation, these transporters can operate in the reverse direction to allow calcium influx and sodium efflux, as an electrogenic mechanism. Structural modelling suggests the presence of 9 TM segments, with a large intracellular loop between the fifth and sixth TM segments.


Author(s):  
Xiaobo Wu ◽  
Gregory S. Hoeker ◽  
Grace Blair ◽  
David Ryan King ◽  
Robert G. Gourdie ◽  
...  

Background: Cardiac voltage-gated sodium channel gain-of-function prolongs repolarization in the Long-QT Syndrome Type 3 (LQT3). Previous studies suggest that narrowing the perinexus within the intercalated disc, leading to rapid sodium depletion, attenuates LQT3-associated action potential duration (APD) prolongation. However, it remains unknown whether extracellular sodium concentration modulates APD prolongation during sodium channel gain-of-function. We hypothesized that elevated extracellular sodium concentration and widened perinexus synergistically prolong APD in LQT3. Methods and Results: LQT3 was induced with anemone toxin type II (ATXII) in Langendorff-perfused guinea pig hearts (n=20). Sodium concentration was increased from 145 to 160 mM. Perinexal expansion was induced with mannitol or the sodium channel β1-subunit adhesion domain antagonist (βadp1). Epicardial ventricular action potentials were optically mapped. Individual and combined effects of varying clefts and sodium concentrations were simulated in a computational model. With ATXII, both mannitol and βadp1 significantly widened the perinexus and prolonged APD, respectively. The elevated sodium concentration alone significantly prolonged APD as well. Importantly, the combination of elevated sodium concentration and perinexal widening synergistically prolonged APD. Computational modeling results were consistent with animal experiments. Conclusions: Concurrently elevating extracellular sodium and increasing intercalated disc edema prolongs repolarization more than the individual interventions alone in the LQT3. This synergistic effect suggests an important clinical implication that hypernatremia in the presence of cardiac edema can markedly increase LQT3-associated APD prolongation. Therefore, this is the first study to provide evidence of a tractable and effective strategy to mitigate LQT3 phenotype by managing patient sodium levels and preventing cardiac edema.


1985 ◽  
Vol 5 (8) ◽  
pp. 667-671 ◽  
Author(s):  
M. S. Suleiman

Decreasing extracellular sodium concentration was found to produce a contractile response of rabbit ileal smooth muscle. As the concentration decreases, the amplitude of contraction increases, thus producing a dose-dependent curve. Harmaline, a competitor for sodium, was found to inhibit the sodium gradient-dependent contractions in a dose-dependent manner. The results are interpreted as harmaline inhibiting a Na–Ca exchange mechanism present in ileal smooth muscle.


1980 ◽  
Vol 88 (1) ◽  
pp. 21-48 ◽  
Author(s):  
BRIJ L. GUPTA ◽  
BETTY J. WALL ◽  
JAMES L. OSCHMAN ◽  
T. A. HALL

1. The concentrations of sodium, potassium and chloride and dry mass were measured by electron-probe X-ray micro-analysis in 1 μm thick frozen-hydrated sections from Calliphora rectum in 5 different states of absorptive function. 2. In all cases the average concentrations of sodium + potassium + chloride was consistently higher in the fluid in the lateral intercellular spaces than in the cytoplasm, the average ratio being 2:1 in water-fed flies and higher in water-deprived flies. 3. The highest concentration of electrolytes was found in the extracellular channel of complex lateral membrane stacks, which is consistent with the histochemical localization of major cation pumps at these sites (Berridge & Gupta, 1968). This concentration exceeded the electrolyte concentration in other tissue compartments by some 80 m-equiv/1 H2O in water-fed flies and about 700 m-equiv/1 H2O in water-deprived flies. The potassium and sodium concentration ratio of this extracellular fluid was nearly 1:1 in water-fed flies, 3:1 in water-deprived flies with KC1 in the rectal lumen, and 0·5:1 with NaCl in the rectal lumen. 4. Results suggest that the extracellular fluid is generated in membrane infoldings along the intercellular channels, and that this fluid gains water and sodium, but loses a variable amount of potassium and chloride, as it passes to the haemolymph, thus supporting the idea of local osmosis and ion recycling.


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