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Endocrine Control of Potassium Balance

David B. Young, Richard D. McCabe

10.1002/cphy.cp070308

Source: Supplement 22: Handbook of Physiology, The Endocrine System, Endocrine Regulation of Water and Electrolyte Balance

Originally published: 2000

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Potassium Transport Along the Nephron
2 Aldosterone: Cellular Mechanisms of Action
2.1 Aldosterone Receptors
2.2 Energetics
2.3 Sodium Conductance
2.4 Hydrogen Ion Transport
2.5 Potassium Transport
2.6 Sodium–Potassium‐Adenosine Triphosphatase
2.7 Chloride Transport
3 Long‐Term Actions of Aldosterone
3.1 Potassium Excretion
3.2 Potassium Distribution
4 Other Hormonal and Nonhormonal Factors that may Affect Potassium Excretion and Distribution
4.1 Sodium Intake and Excretion
4.2 Epinephrine
4.3 Norepinephrine
4.4 Vasopressin
4.5 Insulin
4.6 Angiotensin
4.7 Thyroxin
5 Regulation of Aldosterone Secretion
6 Quantitative Assessments of the Participation of Aldosterone in Potassium Regulation
6.1 Changes in Potassium Intake
6.2 Change in Sodium Intake
6.3 Changes in Aldosterone or Mineralocorticoid Activity
6.4 Potassium Regulation over Combined Ranges of Sodium and Potassium Intake
7 Conclusion
Figure 1. Figure 1.

Renal potassium excretion plotted as a function of plasma potassium concentration under steady‐state conditions. Dogs were adrenalectomized and maintained on normal levels of intravenously infused aldosterone and methylprednisolone. [From Young 248 with permission.]
Figure 2. Figure 2.

Steady‐state relationships between plasma potassium and renal potassium excretion at three levels of aldosterone (Aldo) replacement. [From Young and Paulsen 255 with permission.]
Figure 3. Figure 3.

Three‐dimensional representation of the interaction between plasma potassium and aldosterone in affecting renal potassium excretion. [From Young and Paulsen 255 with permission.]
Figure 4. Figure 4.

Effect of aldosterone (Aldo) on potassium distribution. The relationship between exchangeable potassium (Ke) and plasma potassium (Kp) is rotated downward as the rate of aldosterone replacement is increased from normal (50 μg/day) to five times normal. [From Young and Jackson 252 with permission.]
Figure 5. Figure 5.

Effect of sodium intake on the relationship between plasma potassium concentration and potassium excretion. Increasing sodium intake shifts the relationship up and to the left so that a higher rate of potassium excretion at a given level of plasma potassium would be expected as sodium intake is elevated. [From Young et al. 253 with permission.]
Figure 6. Figure 6.

Three‐dimensional representation of normalized data obtained from Figure 5. Combined effects of sodium intake and plasma potassium on potassium excretion. [From Young et al. 253 with permission.]
Figure 7. Figure 7.

Aldosterone concentration (PAC) as a function of plasma potassium at three levels of angiotensin II infusion on the fifth day of infusion. [From Young et al. 256 with permission.]
Figure 8. Figure 8.

Three‐dimensional presentation of the interaction between normalized angiotensin II concentration and plasma potassium in stimulating aldosterone. Data were obtained from those presented in Figure 7. [From Young et al. 256 with permission.]
Figure 9. Figure 9.

Simulated regulation of plasma potassium concentration over combined ranges of potassium and sodium intake under normal conditions. Grid lines on surface are in increments of 0.25 normalized units. Intake ranges simulated were from 0.25 to 4.0 normal. [From Young 251 with permission.]
Figure 10. Figure 10.

Simulated regulation of plasma potassium concentration over combined ranges of potassium and sodium intake with aldosterone concentration fixed at normal level. Therefore, this surface represents simulated potassium regulation in the absence of feedback regulation of aldosterone levels. Quantitative value of aldosterone in potassium regulation can be appreciated visually by comparing potassium regulation surfaces in this figure with those in Figure 9, in which aldosterone feedback control was normal. [From Young 251 with permission.]


Figure 1.

Renal potassium excretion plotted as a function of plasma potassium concentration under steady‐state conditions. Dogs were adrenalectomized and maintained on normal levels of intravenously infused aldosterone and methylprednisolone. [From Young 248 with permission.]



Figure 2.

Steady‐state relationships between plasma potassium and renal potassium excretion at three levels of aldosterone (Aldo) replacement. [From Young and Paulsen 255 with permission.]



Figure 3.

Three‐dimensional representation of the interaction between plasma potassium and aldosterone in affecting renal potassium excretion. [From Young and Paulsen 255 with permission.]



Figure 4.

Effect of aldosterone (Aldo) on potassium distribution. The relationship between exchangeable potassium (Ke) and plasma potassium (Kp) is rotated downward as the rate of aldosterone replacement is increased from normal (50 μg/day) to five times normal. [From Young and Jackson 252 with permission.]



Figure 5.

Effect of sodium intake on the relationship between plasma potassium concentration and potassium excretion. Increasing sodium intake shifts the relationship up and to the left so that a higher rate of potassium excretion at a given level of plasma potassium would be expected as sodium intake is elevated. [From Young et al. 253 with permission.]



Figure 6.

Three‐dimensional representation of normalized data obtained from Figure 5. Combined effects of sodium intake and plasma potassium on potassium excretion. [From Young et al. 253 with permission.]



Figure 7.

Aldosterone concentration (PAC) as a function of plasma potassium at three levels of angiotensin II infusion on the fifth day of infusion. [From Young et al. 256 with permission.]



Figure 8.

Three‐dimensional presentation of the interaction between normalized angiotensin II concentration and plasma potassium in stimulating aldosterone. Data were obtained from those presented in Figure 7. [From Young et al. 256 with permission.]



Figure 9.

Simulated regulation of plasma potassium concentration over combined ranges of potassium and sodium intake under normal conditions. Grid lines on surface are in increments of 0.25 normalized units. Intake ranges simulated were from 0.25 to 4.0 normal. [From Young 251 with permission.]



Figure 10.

Simulated regulation of plasma potassium concentration over combined ranges of potassium and sodium intake with aldosterone concentration fixed at normal level. Therefore, this surface represents simulated potassium regulation in the absence of feedback regulation of aldosterone levels. Quantitative value of aldosterone in potassium regulation can be appreciated visually by comparing potassium regulation surfaces in this figure with those in Figure 9, in which aldosterone feedback control was normal. [From Young 251 with permission.]

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Article Title: Endocrine Control of Potassium Balance
 

How to Cite

David B. Young, Richard D. McCabe. Endocrine Control of Potassium Balance. Compr Physiol 2011, Supplement 22: Handbook of Physiology, The Endocrine System, Endocrine Regulation of Water and Electrolyte Balance: 306-330. First published in print 2000. doi: 10.1002/cphy.cp070308