Aldosterone secretion is affected by hyperkalemia and hypovolemia, which is a result of reduced extracellular fluid volume (ECFV) due to increased angiotensin II caused by the activation of the renin-angiotensin system (RAS). Conversely, aldosterone secretion is decreased by hypokalemia and natriuretic peptides. This hormone indirectly increases water reabsorption in the collecting duct by stimulating NaCl reabsorption in that specific segment of the nephron.

Interestingly, aldosterone has different effects on the kidneys depending on the condition. When ECFV is depleted, aldosterone levels increase, leading to a reduction in NaCl excretion in order to restore ECFV, without a concurrent change in K+ excretion. On the other hand, in the case of hyperkalemia, aldosterone directly stimulates the release of K+ by the kidneys to normalize plasma K+ levels, but without affecting NaCl excretion. This phenomenon, known as the aldosterone paradox, can be explained by the fact that ECFV depletion activates the RAS and increases aldosterone release, while hyperkalemia directly stimulates the adrenal release of aldosterone without RAS activation. As a result, aldosterone levels increase in both conditions, whereas angiotensin II levels only increase during ECFV depletion and not in hyperkalemia. The aldosterone paradox arises from the differential regulation of transport processes in the distal tubule and collecting duct by aldosterone and angiotensin II. 

During hypovolemia, angiotensin II stimulates NaCl reabsorption in the proximal tubule and early distal tubule by activating WNK (with no lysine [K] kinase), which enhances NaCl reabsorption through the activation of the Na+/Cl- symporter (NCC). Aldosterone, on the other hand, stimulates the reabsorption of Na+ in principal cells of the collecting duct by activating SGK1, which increases the abundance of ENaC in the apical plasma membrane. Additionally, angiotensin II activates WNK in principal cells, inhibiting K+ secretion through ROMK and preventing increased K+ excretion despite elevated aldosterone levels that would typically promote K+ secretion. The stimulation of proximal tubule NaCl and water reabsorption by angiotensin II also reduces the delivery of NaCl and fluid to the collecting duct, thereby suppressing K+ secretion in this segment. The integrated physiological response to a decrease in ECFV is illustrated in Figure 34.10A. Similarly, the corresponding integrated physiological response to hyperkalemia is depicted as well.
Dopamine↑ECFVPT↓H2O and NaCl reabsorptionAVP↑Posm, ↓ECFVDT/CD↑H2O reabsorption aAll these hormones act within minutes, except aldosterone, which exerts its action on reabsorption of NaCl with a delay of 1 hour. Aldosterone achieves its maximal effect after a few days.bThe effect on reabsorption of H2O does not include the thick ascending limb.ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide, BP, blood pressure; CD, collecting duct; DT, distal tubule; ECFV, extracellular fluid volume; [K+]p, plasma K+ concentration; Posm, plasma osmolality; PT, proximal tubule; TAL, thick ascending limb.
Chapter 36]).
Aldosterone secretion is increased by hyperkalemia and by hypovolemia (i.e., reduced ECFV via increased angiotensin II following activation of the renin-angiotensin system [RAS]; see for more details). Aldosterone secretion is decreased by hypokalemia and natriuretic peptides (discussed in more detail next). Through its stimulation of NaCl reabsorption in the collecting duct, aldosterone also indirectly increases water reabsorption by this nephron segment.
The aldosterone paradox. As noted earlier, aldosterone stimulates both NaCl reabsorption and K+ secretion by the collecting duct. Although both a reduction in the ECFV (i.e., hypovolemia, see ) increase aldosterone levels, the physiological response of the kidneys differs in these two conditions. In the setting of ECFV depletion, NaCl excretion by the kidneys is reduced to restore ECFV, without an accompanying change in K+ excretion. By contrast, during hyperkalemia, K+ excretion by the kidneys is increased to normalize plasma [K+], albeit without an accompanying change in NaCl excretion. This phenomenon—the apparent independent effects of aldosterone on urinary Na+ and K+ excretion—is called the aldosterone paradox. The paradox can be explained by the observation that ECFV depletion increases aldosterone release via activation of the RAS, whereas hyperkalemia directly stimulates adrenal release of aldosterone without a requirement for RAS activation. As such, aldosterone increases in both conditions, whereas angiotensin II levels increase only during ECFV depletion and not during hyperkalemia. It is the differential regulation of transport processes in the distal tubule and collecting duct by aldosterone and angiotensin II that accounts for this paradox. The integrated physiological response to a reduction in ECFV is depicted in
Fig. 34.10A . During hypovolemia, angiotensin II stimulates NaCl reabsorption by the proximal tubule (not shown in
Figure 34.10A ), and by the early distal tubule by activating WNK (with no lysine [K] kinase), which enhances NaCl reabsorption by activating the Na+/Cl− symporter (NCC). Aldosterone stimulates ENaC-mediated Na+ reabsorption in principal cells of the collecting duct by activating SGK1, which increases ENaC abundance in the apical plasma membrane. In parallel, angiotensin II activates WNK in principal cells, which inhibits K+ secretion via ROMK, thereby preventing increased K+ excretion despite elevated aldosterone levels, which would be expected to promote K+ secretion. Angiotensin II stimulation of proximal tubule NaCl and water reabsorption also reduces delivery of NaCl and fluid to the collecting duct, which also suppresses K+ secretion in this segment (see for more details). The corresponding integrated physiological response to hyperkalemia is depicted in