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Plasma K+ (mmole/L) Plasma aldosterone (pg/mL) Plasma pH

FIGURE 3 Effects of plasma K+ concentration, plasma aldosterone level, and plasma pH on K+ in the ARDN. The rate of K+ secretion for a single connecting tubule and collecting duct is given. (A) The K+ secretion rate increases sharply with increases in plasma K+ in the range of 4-5.5 mmol/L. (B) Increasing plasma aldosterone concentration also accelerates K+ secretion, and this effect is additive to the effect of a high plasma K+ concentration. (C) When basal K+ secretion is low because of low plasma K+ and aldosterone concentrations, the rate of secretion can be decreased by acidemia and increased by alkalemia. (Modified from Wright FS, Giebisch G. Regulation of K+ excretion. In Seldin DW, Giebisch G, eds. The kidney: Physiology and pathophysiology. New York: Raven Press, 1985, pp 1223-1249.)

augments Na+ reabsorption, also leads to increased K+ secretion. Therefore, dehydration is often associated with increased K+ excretion that can lead to significant depletion of body K+ stores.

Acute respiratory and metabolic acid-base disturbances also affect renal K+ excretion. As shown in Fig. 3C, alkalosis is associated with increased K+ secretion, whereas acidosis is associated with decreased K+ secretion by CNT and principal cells of the ARDN. Part of this effect may be due to the change in intracellular K+ concentration with changes in plasma pH. The shift of K+ into cells in alkalosis could increase the concentration driving force for K+ secretion, with the reverse occurring in acidosis. However, there is also a direct effect of pH on the K+ channels in the luminal membrane of the principal cell—alkalosis stimulates and acidosis inhibits them. Chronic acid-base disturbances produce complex changes in K+ secretion, which will be discussed in Chapter 31.

Factors Affecting K+ Secretion by the Aldosterone-Responsive Distal Nephron

As discussed in Chapter 27 and in the Clinical Note on the effects of diuretics in that chapter, K+ secretion is also considerably enhanced when the delivery of Na+ or fluid flow through the connecting tubule and collecting duct (the ARDN) is increased. Because of the clinical importance of this effect, it is worthwhile to consider again the mechanism responsible for K+ secretion in the

ARDN, which is illustrated in Fig. 4. (This figure has been adapted from Fig. 5 in Chapter 27 to highlight the K+ secretory mechanism.) K+ is secreted from CNT and principal cells into the tubular fluid by moving passively down its electrochemical potential gradient through K+-selective channels in the luminal membrane. There is a driving force for K+ to leave the cell where its concentration is higher than in the tubular fluid. Furthermore, because of the Na+ permeability of the luminal membrane, the voltage across the membrane is less negative from cell to lumen (—30 mV) than across the basolateral membrane (—80 mV). This lower opposing negative voltage gives a larger net electrochemical potential driving force for K+ to leave the cell across the luminal membrane. Thus, three factors influence the rate of K+ secretion: the intracellular K+ concentration, the luminal K+ concentration, and the voltage across the luminal membrane. When intracellular K+ is reduced, secretion decreases because the concentration difference across the luminal membrane decreases. With increased luminal flow rate, K+ secretion increases because the K+ concentration in the lumen remains lower (due to the larger volume of fluid) despite a higher K+ secretion rate. Although the luminal K+ concentration remains lower, the final excretion of K+ is greater because the flow rate is greater. Increased Na+ delivery to the distal tubule also tends to enhance K+ secretion. With an increased Na+ concentration in the lumen, greater depolarization of the luminal membrane is seen, resulting in a lower opposing voltage and, thus, a greater

FIGURE 4 Driving forces for K+ secretion by CNT and principal cells of the ARDN. A high intracellular K+ concentration is maintained by the Na+,K+-ATPase, which provides a favorable concentration gradient for K+ to diffuse through K+ channels in the luminal membrane. The voltage difference across the luminal membrane (-30 mV, cell compared to lumen) is also less than that across the basolateral cell membrane (-80 mV, cell compared to interstitial fluid) because it is depolarized by the Na+ channels (not shown in this diagram). Thus, there is less of an electrical force retarding K+ movement into the lumen. The net result is a favorable electrochemical potential gradient for K+ to diffuse from the cells into the lumen resulting in secretion.

FIGURE 4 Driving forces for K+ secretion by CNT and principal cells of the ARDN. A high intracellular K+ concentration is maintained by the Na+,K+-ATPase, which provides a favorable concentration gradient for K+ to diffuse through K+ channels in the luminal membrane. The voltage difference across the luminal membrane (-30 mV, cell compared to lumen) is also less than that across the basolateral cell membrane (-80 mV, cell compared to interstitial fluid) because it is depolarized by the Na+ channels (not shown in this diagram). Thus, there is less of an electrical force retarding K+ movement into the lumen. The net result is a favorable electrochemical potential gradient for K+ to diffuse from the cells into the lumen resulting in secretion.

K+ secretion. In summary, diuretics enhance K+ secretion in the ARDN by providing a larger volume of fluid into which the K+ is secreted, as well as by producing a more negative luminal voltage, both of which enhance the electrochemical potential gradient down which K+ leaves the cell.

Finally, the rate of delivery of anions other than Cl-to the distal tubule is also an important determinant of K+ secretion. K+ secretion is enhanced when poorly reabsorbed anions are present in the tubular fluid, probably because less salt and water are reabsorbed. The loss of K+ via this route can become quite acute, for example, in diabetic ketoacidosis, in which large amounts of acetoacetate and ^-hydroxybutyrate are delivered to the distal tubule and collecting duct.

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