Introduction.
Maintenance of potassium balance is vitally important for normal nerve and muscle function. Both deficits and surfeits of potassium disturb the electrical activity of excitable membranes by altering the ratio of extracellular K concentration to the intracellular concentration (K_o/K_i) and by affecting membrane conductance to K. This can lead to skeletal and smooth muscle weakness and paralysis and profound disturbance of cardiac function.

A. Ninety percent of the body's content of potassium is contained within cells, principally muscle cells, and is readily exchangeable (Fig. 10-1). Only 2.5% is found in the ECF; most of the rest is contained in bone. The normal daily dietary intake of potassium is roughly equivalent to the small fraction of total body K contained in the ECF. The kidney is the major organ responsible for K excretion and for the long term regulation of K balance. The colon excretes a small fraction of the daily intake.

Fig. 10-1. Schematic representation of total body potassium distribution and the maintenance of potassium homeostasis.

B. An episodic intake of a large K load (e.g., a large high-protein meal) could potentially cause a life-threatening doubling of the extracellular K concentration. Similarly, a short period of time in which renal output of K exceeds the intake could produce a dangerous reduction of the extracellular concentration. However, short term shifts of K across cell membranes can protect the extracellular concentration from large changes while causing only small fractional changes in the cellular concentration. In this way changes in the K_o/K_i ratio are minimized.

C. A number of humoral factors act on muscle and other extrarenal tissue to maintain plasma K levels by shifting K in and out of the cellular compartment. Other factors such as acid-base balance can affect the balance between cellular and extracellular K concentrations.

1. Insulin directly stimulates Na-K ATPase in liver and muscle cell membranes so that K uptake into the cell is increased. This effect of insulin is important in the daily regulation of K balance. The stimulation of insulin secretion associated with the ingestion of food causes K in the ECF to be shifted into cells preventing a large change in ECF K concentration as the K in the food is absorbed from the G.I. tract. Large increases in ECF K concentration (>1-1.5 mEq/l) stimulate insulin secretion and this promotes movement of the excess K into the intracellular compartment.

2. Aldosterone acts on extrarenal as well as renal cells to increase the uptake of K into the cell. The effect of aldosterone is slower than that of insulin. The effect of the hormone on the kidney and on extrarenal cells is important in maintaining K balance in the long term. However, the slowness of its effect prevents it from playing a role in the hour-to-hour maintenance of K balance.

3. -2 receptors on muscle cells respond to catecholamines by indirectly stimulating the Na-K pump. There is no good evidence that the plasma K concentration affects catecholamine secretion. However a number of situations, such as food intake, increased muscle activity, etc., are associated with increased catecholamine levels and increases in plasma K concentration. The effect of the catecholamines on K uptake by cells limits the rise in plasma K in these situations.

4. Acidosis increases the plasma K concentration by inducing a net shift of K from the cellular to the extracellular compartment.

QUESTIONS:  
1. What is the effect of a rise in the K_o/K_i on the resting membrane potential and excitability of muscle and nerve cells? What is the effect of increasing plasma K concentration by 5 mEq/l?

2. In treating a patient with chronic hypokalemia, is there any problem associated with repairing that deficiency by intravenous infusion of a solution with a high K concentration?

3. In treating a life-threatening episode of hyperkalemia, an injection of insulin, glucose and NaHCO₃ is often administered? What is the rationale for this?

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