Review of Medical Physiology - William F. Ganong 2002

Urine Formation and Excretion
Renal Function and Micturition
Regulation of K+ Excretion

A significant portion of K⁺ is removed from the tubular fluid via active reabsorption in the proximal tubules (see Table 38-5). Subsequently, K⁺ is secreted into the tubular fluid by the Cells of the distal nephron. The rate of K⁺ secretion is proportional to the flow rate of the tubular fluid through the distal segments of the nephron, because rapid fluid passage through the tubules makes it less likely that the K⁺ concentration in the tubular fluid will rise to a level that halts further secretion. Absent any interfering factors, The amount of K⁺ secreted roughly equals the external K⁺ intake, thereby maintaining potassium balance. In the distal tubule, Na⁺ is predominantly reabsorbed, whereas K⁺ is secreted. There is no strict one-for-one exchange here, and the bulk of K⁺ movement occurs via passive mechanisms. However, the influx of K⁺ into the cells reduces the bioelectric potential difference across the tubular Cell membrane, which in turn facilitates the movement of K⁺ ions in the opposite direction—namely, into the tubular lumen. Because Na⁺ reabsorption is also coupled with H⁺ secretion, a competitive mechanism resembling Na⁺ trapping takes place in the tubular fluid. K⁺ excretion slows down when the amount of Na⁺ in the tubular fluid decreases at the level of the distal tubule, as well as when H⁺ secretion increases. When total body K⁺ content is high, H⁺ secretion is inhibited, presumably due to intracellular alkalosis; under these conditions, K⁺ secretion and excretion are significantly enhanced. Conversely, in cases of K⁺ deficit, intracellular acidosis develops and K⁺ secretion ceases. The K⁺ secretion mechanism possesses the capacity for adaptation, as evidenced by the fact that prolonged administration of large doses of potassium salts leads to a progressive increase in K⁺ excretion.

Hypokalemia is a fairly common condition that can have serious consequences. Besides excessive urinary loss of K⁺, this state is sometimes caused by gastrointestinal K⁺ losses resulting from prolonged diarrhea, as well as the intracellular shift of K⁺ from Blood Plasma in patients receiving Insulin (see Chapter 19) or ß-blockers, and, naturally, in cases of chronically low dietary K⁺ intake. Hyperkalemia is a much more dangerous condition than hypokalemia due to potentially life-threatening cardiovascular complications (see Chapter 28). Nevertheless, in the presence of normal renal function, hyperkalemia is rarely observed.