Effects of abamectin on intracellular potassium ion activity and membrane potential in dipteran skeletal muscle

1993 ◽  
Vol 37 (1) ◽  
pp. 49-55
Author(s):  
Elizabeth M. Fitzgerald ◽  
Jason Curry ◽  
Mustafa B. A. Djamgoz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Potassium Ion ◽  
Intracellular Potassium ◽  
Ion Activity

Intracellular potassium ion activity in resting and stimulated mouse pancreas and submandibular gland

1979 ◽  
Vol 204 (1154) ◽  
pp. 99-104 ◽  
Keyword(s):  
Submandibular Gland ◽  
Marked Decrease ◽  
Potassium Ion ◽  
Pancreatic Acinar Cells ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Mouse Pancreas ◽  
Intracellular Potassium ◽  
Ion Activity ◽  
Ion Activities

Intracellular potassium ion activities ( a i K + ) and membrane potentials were measured with double-barrelled, potassium-specific microelectrodes in superfused mouse pancreas and submandibular gland. Stimulation with the cholinergic agonist bethanechol caused a marked decrease in a i K + in the submandibular gland, whereas no change in a i K + could be detected in the pancreas. This indicates that bethanechol increases the permeability of the cell membranes to potassium ions in the submandibular gland but not in the pancreas. Pancreatic acinar cells hyperpolarized promptly when the extracellular potassium ion activity was restored after a prolonged period of potassium deprivation. In comparison, the recovery of a i K + was a slow process. This finding gives support to the view that the hyperpolarization is due to electrogenic sodium pumping.

scholarly journals Reversible changes in the intracellular potassium ion activities and membrane potentials of Aplysia L2-L6 neurones in response to normoxia and hypoxia

1983 ◽  
Vol 102 (1) ◽  
pp. 79-92
Author(s):  
P. E. Coyer ◽  
J. H. Halsey ◽  
E. R. Strong
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Membrane Potentials ◽  
Potassium Ion ◽  
Intracellular Potassium ◽  
Goldman Equation ◽  
Ion Activities

1. Exposure of 7 L2-L6 neurones to hypoxia for 65 min resulted in hyperpolarization of the membrane potential (EM) from a mean of −49.1 +/− 2.1 to −54.1 +/− 3.6 mV (S.E.). 2. Intracellular potassium ion activities (aiK) increased significantly from 137.7 +/− 4.0 to 155.6 +/− 3.4 mM-K+. This is equivalent to a change in EK from −74.2 mV commensurate with the observed hyperpolarization of 5 mV. 3. The reversibility of these responses was noted by reoxygenating the solution surrounding the ganglion for a period of 55 min. 4. In another group (n = 7) of L2-L6 neurones, the responses in aiK, EM, and EK were slower, although following hypoxia for 90–110 min, similar changes in the levels of these membrane phenomena were recorded. 5. PNa/PK ratios were computed for both L2-L6 groups of neurones using a modified version of the Goldman equation. There were only slight decreases in this ratio with hypoxia, which were not significantly different from the control (normoxia). Therefore, we conclude that this period of hypoxia is capable of stimulating the sodium pump of these cells since the membrane potentials seem to hyperpolarize according to the increase in aiK. However, tonic release of neurotransmitter, which could hyperpolarize these neurones and attract intracellular potassium, cannot be ruled out as an effect of hypoxia.

scholarly journals Dose Response of Endotoxin on Hepatocyte and Muscle Mitochondrial Respiration In Vitro

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Victor Jeger ◽  
Sebastian Brandt ◽  
Francesca Porta ◽  
Stephan M. Jakob ◽  
Jukka Takala ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Mitochondrial Respiration ◽  
Hepg2 Cells ◽  
Human Hepatocytes ◽  
Atp Content ◽  
Muscle Mitochondria ◽  
Complex Ii ◽  
Skeletal Muscle Mitochondria ◽  
Reduced Time

Introduction.Results on mitochondrial dysfunction in sepsis are controversial. We aimed to assess effects of LPS at wide dose and time ranges on hepatocytes and isolated skeletal muscle mitochondria.Methods.Human hepatocellular carcinoma cells (HepG2) were exposed to placebo or LPS (0.1, 1, and 10 μg/mL) for 4, 8, 16, and 24 hours and primary human hepatocytes to 1 μg/mL LPS or placebo (4, 8, and 16 hours). Mitochondria from porcine skeletal muscle samples were exposed to increasing doses of LPS (0.1–100 μg/mg) for 2 and 4 hours. Respiration rates of intact and permeabilized cells and isolated mitochondria were measured by high-resolution respirometry.Results.In HepG2 cells, LPS reduced mitochondrial membrane potential and cellular ATP content but did not modify basal respiration. Stimulated complex II respiration was reduced time-dependently using 1 μg/mL LPS. In primary human hepatocytes, stimulated mitochondrial complex II respiration was reduced time-dependently using 1 μg/mL LPS. In isolated porcine skeletal muscle mitochondria, stimulated respiration decreased at high doses (50 and 100 μg/mL LPS).Conclusion.LPS reduced cellular ATP content of HepG2 cells, most likely as a result of the induced decrease in membrane potential. LPS decreased cellular and isolated mitochondrial respiration in a time-dependent, dose-dependent and complex-dependent manner.

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