An increase in aldosterone levels enhances the activity of Na+,K+-ATPase, but it doesn't immediately increase K+ excretion. This is because aldosterone also stimulates the reabsorption of Na+ and water, which decreases tubular flow and subsequently reduces K+ secretion. However, chronic stimulation of Na+ reabsorption restores tubular flow to normal by increasing the extracellular fluid volume (ECFV). This allows aldosterone to directly enhance K+ excretion in the aldosterone-sensitive distal nephron (ASDN).

Although vasopressin (AVP) does not affect urinary K+ excretion, it promotes K+ secretion by the ASDN. AVP increases the electrochemical driving force for K+ exit across the apical membrane of principal cells by stimulating Na+ uptake through the same membrane. This reduces the electrical potential difference across the apical membrane. Despite this effect, AVP does not change K+ secretion by the ASDN. This is because AVP decreases the flow of tubular fluid by promoting water reabsorption, which in turn reduces K+ secretion.

If AVP didn't increase the electrochemical gradient favoring K+ secretion, urinary K+ excretion would decrease as AVP levels increase and urinary flow rates decrease. Therefore, the inhibitory effect of decreased tubular fluid flow offsets the stimulatory effect of AVP on the electrochemical driving force for K+ secretion. This enables K+ balance to remain constant despite changes in water excretion.

Plasma potassium concentration [K+], aldosterone, and AVP all play important roles in regulating K+ balance. However, other factors and hormones can disrupt K+ balance. For example, an increase in tubular fluid flow stimulates K+ secretion within minutes, while a decrease in flow reduces K+ secretion by the late segment of the ASDN. The effectiveness of flow in stimulating K+ secretion is greater with higher dietary K+ intake. Recent studies have revealed some of the mechanisms through which increased flow stimulates K+ secretion, particularly involving the primary cilium in principal cells.
Although an acute (e.g., within hours) increase in aldosterone levels enhances the activity of Na+,K+-ATPase, K+ excretion does not increase immediately. The reason for this relates to the effect of aldosterone on Na+ reabsorption and tubular flow. Aldosterone stimulates reabsorption of Na+ and water and thus decreases tubular flow. Reduction in flow in turn decreases K+ secretion (as discussed in more detail later). However, chronic stimulation of Na+ reabsorption increases the ECFV and thereby returns tubular flow to normal. These actions allow a direct stimulatory effect of aldosterone on the ASDN to enhance K+ excretion.
Although AVP does not affect urinary K+ excretion, this hormone does promote secretion of K+ by the ASDN (Fig.
36.8 ). AVP increases the electrochemical driving force for exit of K+ across the apical membrane of principal cells by stimulating uptake of Na+ across the apical membrane of these cells. The increased Na+ uptake reduces the electrical potential difference across the apical membrane (i.e., the interior of the cell becomes less negatively charged). Despite this effect, AVP does not change K+ secretion by these nephron segments. The reason for this relates to the effect of AVP on tubular fluid flow. AVP decreases flow of tubular fluid by stimulating water reabsorption. The decrease in tubular flow in turn reduces secretion of K+ (explained later). The inhibitory effect of decreased flow of tubular fluid offsets the stimulatory effect of AVP on the electrochemical driving force for exit of K+ across the apical membrane (see
Fig. 36.8 ). If AVP did not increase the electrochemical gradient favoring K+ secretion, urinary K+ excretion would fall as AVP levels increased and urinary flow rates decreased. Hence K+ balance would change in • Fig. 36.8 Opposing effects of AVP and urine flow rate on secretion of K+by the ASDN. K+secretion is stimulated by an increase in urinary flow rate and reduced by a fall in AVP levels. In contrast, K+secretion is reduced by a decrease in urinary flow rate and increased by a rise in AVP levels. Because the effects of flow and AVP oppose each other, net K+secretion is not affected by water diuresis or antidiuretics. ˜ Urinary flow rate Water diuresis DT/CCD K+ secretion ˛ AVP levels Constant K+ balance ˛ Urinary flow rate DT/CCD K+ secretion ˜ AVP levels Antidiuresis + _ _ + response to alterations in water balance. Thus the effects of AVP on the electrochemical driving force for exit of K+ across the apical membrane and on tubule flow enable urinary K+ excretion to be maintained constant despite wide fluctuations in water excretion.
Plasma [K+], aldosterone, and AVP play important roles in regulating K+ balance; however, the factors and hormones discussed next perturb K+ balance (see
Box 36.2
Flow of Tubular Fluid
A rise in the flow of tubular fluid (e.g., with diuretic treatment, ECFV expansion) stimulates secretion of K+ within minutes, whereas a fall (e.g., ECFV contraction caused by hemorrhage, severe vomiting, or diarrhea) reduces secretion of K+ by the late segment of the ASDN. Increments in tubular fluid flow are more effective in stimulating secretion of K+ as dietary K+ intake is increased. Recent studies on the primary cilium in principal cells have elucidated some of the mechanisms whereby increased flow stimulates secretion of K+ (