Potassium, intracellular depletion

Both intracellular depletion of potassium and hypertonic treatment lead to disruption of clathrin from the inner side of the plasma membrane. Consequently, the formation of clathrin-coated pits and clathrin-coated vesicles is... 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Andersson, B. Janson, V. Behnam-Motlagh, R Henriksson, R. Grankvist, K. Induction of apoptosis by intracellular potassium ion depletion using the fluorescent dye PBFI in a 96-well plate method in culmred lung cancer cells. Toxicol. In Vitro 2006, 20, 986-994. 

Reversible electrocardiographic (EKG) T-wave depression occurs frequently with therapeutic serum lithium concentrations. Arrhythmias have occurred rarely. The cardiac effects of lithium may result partly from displacement of potassium from intracellular myocardial sites by lithium, resulting in a slow, partial depletion of intracellular potassium (Kawata, 1979). 

Acridine dyes used as antiseptics, i.e. proflavine and acriflavine, will react specifically with nucleic acids, by fitting into the double helical structure of this unique molecule. In so doing they interfere with its function and can thereby cause cell death. There is evidence that a depletion of intracellular potassium caused by membrane damage can lead to the activation of latent ribonucleases and the consequent breakdown of RNA. Several biocides, including cetrimide and some phenols, are known to cause the release of nucleotides and nucleosides following an autolytic process. This is irreversible and has been proposed as an autocidal (suicide) process, committing the injured cell to death (Denyer Stewart, 1998). 

The main determinant of citrate excretion is probably the intracellular pH of the tubular cells (Cll, HIO, M25), as is shown by the fact that urinary citrate decreases in potassium depletion (F9), as well as after administration of maleic acid (H9) or acetazoleamide (G15, G16, HIO, OH), which produces a metabolic acidosis associated with an alkaline urine. 

D. Metabolic effects include hypokalemia, hyperglycemia, and lactic acidosis. Hypokalemia is caused by an intracellular shift of potassium rather than true depletion. 

C. Potassium depletion resulting in a 1-mEq/L decrease in serum potassium may require 100-200 mEq tor replacement to restore body stores. This replacement requirement will be offset with changes or corrections in intracellular transport (reversal of methyixanthine or beta-adrenergic agonist toxicity). 

Potassium. Draw a diagram as you proceed through this paragraph. As a result of the renal effects, the body is (depleted of, loaded with) potassium and the plasma potassium is (high, low). Consequently, potassium will tend to (leave, enter) the cells of the body. To maintain electrochemical neutrality, this will lead to hydrogen ions (entering, leaving) the cells so that the extracellular-metabolic alkalosis is (exacerbated, returned towards normal). There is an intracellular (acidosis, alkalosis). 

In potassium depletion (e.g. Cushing s syndrome, aldosteronism). Potassium depletion in the extracellular fluid causes K+ to move out of the cells, and this is accompanied by a movement of and Na" into the cells. This results in an extracellular alkalosis (although there is at the same time an intracellular acidosis). 

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