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Renal Potassium Transport

Bruce A. Stanton, Gerhard H. Giebisch

10.1002/cphy.cp080119

Source: Supplement 25: Handbook of Physiology, Renal Physiology

Originally published: 1992

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 External and Internal Potassium Balance
1.1 Internal Potassium Balance
1.2 External Potassium Balance
2 General Features of Renal Potassium Excretion
3 Cellular Mechanisms of Potassium Transport Along the Nephron
3.1 Glomerulus
3.2 Proximal Tubule
3.3 Loop of Henle
3.4 Potassium Recycling
3.5 Distal Tubule
3.6 Distal Convoluted Tubule
3.7 Connecting Tubule
3.8 Initial Collecting Tubule and Cortical Collecting Duct
3.9 Medullary Collecting Duct
3.10 Inner Medullary Collecting Duct
3.11 Amphibian Distal Nephron
4 Regulation of Potassium Transport
4.1 Potassium Intake and Plasma Potassium Concentration
4.2 Potassium Adaptation
4.3 Adrenal Steroids
5 Regulation of Potassium Excretion by Interactive Stimuli
5.1 Relationship between Plasma Potassium Concentration, Plasma Aldosterone, and Renal Potassium Excretion
5.2 Effects of Sodium Intake on Potassium Balance
5.3 Regulation of Potassium and Sodium Excretion during Alterations in Extracellular Fluid Volume
5.4 Regulation of Potassium and Sodium Excretion during Alterations in Potassium Intake
Figure 1. Figure 1.

Potassium homeostasis depends on maintenance of external and internal potassium balance. External potassium balance is determined by rate of potassium intake (100 mEq/day) and rate of urinary (90 mEq/day) and fecal excretion (10 mEq/day). Internal potassium balance depends on distribution of potassium between muscle, bone, liver, and red blood cells (RBC) and the extracellular fluid (ECF). This distribution is regulated by several hormones and is affected by acid–base balance and tonicity of plasma. (Movement of potassium between the ECF and cells is indicated by the small arrows; see text for details.)
Figure 2. Figure 2.

Schematic illustration of superficial (right) and juxtamedullary (left) nephrons in mammalian kidney. Arrows indicate direction of potassium transport. Abbreviations: CNT, connecting tubule; DCT, distal convoluted tubule; PCT, proximal convoluted tubule; PST, proximal straight tubule (the entire proximal tubule can also be divided into three segments labeled S1, S2, S3); TAL, thick ascending limb; DTL, descending thin limb; ATL, ascending thin limb; ICT, initial collecting tubule; CCD, cortical collecting duct; TAL, thick ascending limb; OMCDo, outer medullary collecting duct (outer stripe); OMCDi, outer medullary collecting duct (inner stripe); IMCDi, inner medullary collecting duct (initial segments); IMCDt, inner medullary collecting duct (terminal segment).
Figure 3. Figure 3.

Schematic illustration of cell types lining distal tubule and cortical collecting duct in rat. Transitions between distal convoluted tubule (DCT), connecting tubule (CNT), and initial collecting duct (ICT) are gradual in the rat and the human but more abrupt in the rabbit.

from 419
Figure 4. Figure 4.

Koefoed‐Johnson—Ussing cell model of sodium transport across frog skin (modified from 245). As discussed in the text, inclusion of additional potassium transport mechanisms in the apical and/or basolateral membrane can account for potassium transport processes observed along the nephron. Apical solution is electrically negative relative to a grounded bath solution.
Figure 5. Figure 5.

Potassium transport mechanisms in renal cells. Direction and magnitude of potassium transport in each nephron segment is integrally related to distribution of one or more of these mechanisms to apical or basolateral membrane.
Figure 6. Figure 6.

Proximal cell model of potassium transport. Transepithelial voltage is lumen‐negative in early convolutions and lumen‐positive in late convolutions (relative to a grounded bath solution). Potassium conductance of the apical membrane is small relative to the potassium conductance of the basolateral membrane. According to this model, which incorporates all known potassium‐transport mechanisms, transcellular potassium movement can only occur in the secretory direction. As noted in the text, however, potassium is normally absorbed by the proximal tubule. Transcellular potassium absorption requires an active uptake mechanism in the apical membrane (not shown); see text for details.
Figure 7. Figure 7.

Expanded cell model to account for active potassium absorption by proximal tubule. Cellular potassium absorption may be driven by Na+,K+‐ATPase in lateral membranes, which lowers potassium concentration in interspace and provides driving force for potassium diffusion across tight junction from tubular lumen into interspace. Some potassium may then cross basement membrane by solvent drag. Potassium that enters cell via Na+,K+‐ATPase across lateral membrane preferentially diffuses out of cell across basal membrane through potassium channels. For this mechanism to work, potassium diffusion from cell into lateral interspace and from interspace into tubular lumen must be relatively small; see the text for details.

Modified from 478,480
Figure 8. Figure 8.

Model of descending thin limb of Henle's loop illustrating known potassium transport pathways (modified from 281). Potassium transport may either be in the secretory or absorptive direction depending on the orientation of potassium transepithelial concentration gradient.
Figure 9. Figure 9.

Model of cells of thick ascending limb of Henle's loop illustrating known potassium‐transport pathways. Transepithelial voltage is oriented lumen‐positive relative to a grounded bath solution. Cl−− exchanger has been described in apical membrane of mouse thick ascending limb cells 109. This mechanism, in parallel with Na+−H+ exchanger, would mediate electroneutral NaCl absorption 109. Operation of the Cl−− transporter in concert with the Na+−H+ exchanger would reduce or eliminate sodium‐induced changes in intracellular pH.

Modified from 109
Figure 10. Figure 10.

Potassium recycling. Arrows depict route of potassium recycling within renal medulla.
Figure 11. Figure 11.

Cell model of distal convoluted tubule illustrating known potassium‐transport pathways. KCl cotransport mechanism and potassium‐conductive pathway (not shown) mediate potassium secretion across apical membrane. These potassium‐transport pathways are in parallel with a NaCl cotransport mechanism and a sodium conductive pathway. Transepithelial voltage is oriented lumen‐negative relative to a grounded bath solution.
Figure 12. Figure 12.

Model illustrating known potassium‐transport pathways of principal cells in initial and cortical collecting duct.

see text for details
Figure 13. Figure 13.

Current record of potassium channel in apical membrane of principal cells from rabbit cortical collecting duct. Record was obtained in the cell‐attached configuration with 70 mM NaCl and 70 mM KCl (pH 7.4, Ca2+ free) in the bath and 140 mM KCl in the pipette at 37°C. Closed state is indicated by “C,” and clamp voltage is indicated on left side of the figure. Downward deflection is inward current; upward deflection, outward current.

from 468
Figure 14. Figure 14.

Known hormones and elements regulating small‐conductance apical potassium channel, basolateral potassium channels, and apical sodium channels in principal cells of the cortical collecting duct.

Modified from ref. 475
Figure 15. Figure 15.

Model of the acid‐secreting intercalated cell type in the collecting duct illustrating possible mechanisms of potassium absorption. Potassium may be absorbed via a K+,H+‐ATPase located in the apical membrane. This mechanism may be expressed only during potassium depletion. The mechanism of potassium exit from the cell into the blood is unknown. An H+‐ATPase is also present in the apical membrane. It is not known whether H+‐ATPase and H+,K+‐ATPase are both present in control and potassium‐depleted states.
Figure 16. Figure 16.

Model of inner medullary collecting duct cell (initial segment) illustrating potassium transport pathways. Sodium uptake across apical membrane is mediated by amiloride‐sensitive cation channel (Pna/Pk = 1) in initial segment. In terminal segment, apical membrane does not contain significant conductive pathway for sodium. Potassium transport by this segment may be exclusively paracellular, or may occur via cellular pathway. Cellular route requires potassium transport mechanism in apical membrane. Because cation channel is also conductive to potassium, secretion may occur via this pathway when potassium concentration in tubular fluid is low. The Na+−2Cl−−K+ cotransport mechanism in basolateral membrane is present only in rat 147,362.
Figure 17. Figure 17.

Relationship between plasma potassium concentration and potassium secretion by rat distal tubule perfused in vivo at constant flow rate. Potassium was infused intravenously over 4 hours.

from 420
Figure 18. Figure 18.

Effects of potassium (k+), aldosterone (Aldo), k+, and Aldo and dexamethasone (Dex) on potassium secretion (JK; top panel) by distal tubules, urinary potassium excretion (UKV; bottom panel), and urine flow rate (V middle panel).

from 102
Figure 19. Figure 19.

Effect of increased plasma potassium levels on potassium secreting by distal tubule (JK) in control and K‐adapted rats. Potassium‐adapted rats were fed high potassium diet for 2–4 weeks; open bars, plasma potassium 4 mEq/liter: hatched bars, plasma potassium about 7 mEq/liter. Control tubules secreted less potassium than tubules from potassium‐adapted animals. When challenged with an acute K+ load, control animals increased K excretion modestly, although plasma K+ rose to about 7 mEq/liter. In contrast, administration of similar K+ load to K+‐adapted animals led to sharp increase of K+ secretion, although plasma potassium increased less than that in control animals.

Data from 419,420
Figure 20. Figure 20.

Relationship between whole body potassium content as function of plasma potassium levels in adrenalectomized dogs given normal or high aldosterone (5X). Note that for a given amount of exchangeable potassium, a larger fraction of potassium is sequestered inside cells as aldosterone levels increase. [Modified from 469.] At any plasma potassium level, aldosterone reduces total body potassium.
Figure 21. Figure 21.

Time course of “DOCA‐escape” phenomenon. Aldosterone (Aldo) administration increases sodium and fluid absorption by distal tubule and cortical collecting duct (Phase 1), which leads to volume expansion. Sodium “escapes” from sodium retaining effects because of pressure natriuresis (Phase 2);.

from 100
Figure 22. Figure 22.

Transmission electron micrographs illustrating chronic effect of high‐potassium diet on ultrastructure of principal cells in initial and cortical collecting duct. A. Control. B. K+‐adapted animal given a high‐K+ diet for 4 weeks. Bar equals 1 μm (from 419).
Figure 23. Figure 23.

Effects of chronic DOCA treatment (5 mg/day) on electrophysiological and biochemical properties of cortical collecting ducts isolated from adrenal‐intact rabbits. Data in top and middle panels calculated by equivalent circuit analysis. Top: apical membrane sodium () and potassium () current. Middle: apical membrane potassium () and sodium () conductance. Bottom: activity of Na+,K+‐ATPase.

modified from 332
Figure 24. Figure 24.

Effects of chronic (6–10 days) DOCA treatment on transepithelial voltage (Vte) and driving forces for potassium transport across apical (Va−EK) and basolateral (Vbl−EK) membrane of principal cells in isolated rabbit cortical collecting ducts. The negative value of Va−EK for control and DOCA tubules indicates that potassium diffuses out of the cell into the tubule lumen. With regard to Vbl−EK in control tubules, positive value indicates that potassium diffuses out of cell into blood. In DOCA tubules the driving force reverses such that potassium now enters cells from blood through potassium channels in the basolateral membrane.

modified from 372
Figure 25. Figure 25.

Effects of DOCA on the electrophysiological properties of principal cells in the cortical collecting duct from adrenalectomized rabbits. Top: effects of amiloride on DOCA‐induced changes in sodium () and potassium () currents across apical membrane. Bottom: effects of amiloride on DOCA‐induced changes in potassium () and sodium () conductance of apical membrane.

data from 373
Figure 26. Figure 26.

Equivalent circuit diagram illustrating effects of high‐K+ diet on the electrophysiological properties of the cell membranes and the paracellular pathway in adrenalectomized rabbits. INa = sodium current; IK = potassium current; Gtj = conductance of the tight junction; = sodium conductance of the apical membrane, = potassium conductance of the apical membrane; ENa = Nernst equilibrium potential of sodium; EK = Nernst equilibrium potential of potassium; Va = voltage across apical membrane; Vte = transepithelial voltage; Vb = voltage across basolateral membrane; Ki = intracellular potassium activity; Gb = basolateral membrane conductance, IP max = current through Na+,K+‐ATPase. Currents expressed as μA/cm2, conductance as mS‐cm2 and voltage in mV.

data from 320
Figure 27. Figure 27.

Relationship between tubule perfusion rate and tubular fluid‐to‐potassium concentration ratios ([K+] TF/P) in late distal tubule perfused in vivo from control, low K, and K‐adapted rats.

From 287
Figure 28. Figure 28.

A. Relationship between tubule flow rate and potassium secretion (JK) by rat distal tubules as measured by free‐flow micro‐puncture and tubule perfusion. Relationship between flow and secretion is steeper in free‐flow conditions, except when flow is below 1.5 nl/min. B. Relationship between tubule flow rate and sodium absorption (JNa) in rat distal tubules as measured by free‐flow and tubule perfusion. Relationship is steeper in free‐flow conditions because sodium concentration in tubule fluid increased as flow increased whereas the sodium concentration was unchanged in perfusion experiments.

from 287
Figure 29. Figure 29.

Relationship between tubule perfusion rate and potassium secretion () by isolated rabbit cortical collecting ducts. Solid line and filled circles: data from tubules harvested from animals on a control diet. Open line and open circles: data from tubules harvested from animals with elevated aldosterone levels.

data from 95
Figure 30. Figure 30.

Effects of sodium concentration in tubular lumen ([Na]L) on potassium secretion and transepithelial voltage across perfused rat distal tubules (a, b) and isolated perfused rabbit cortical collecting ducts (c, d).

Data from 133,134,135,423
Figure 31. Figure 31.

Transmission electron micrographs of principal cells in cortical collecting duct of rat. A. Control. B. After 6 days of enhanced sodium delivery into the collecting duct produced by furosemide infusion. Note the cell hypertrophy and selective proliferation of basolateral membrane.

from 222
Figure 32. Figure 32.

Relationship between plasma potassium concentration and urinary potassium excretion in dog. Alkalosis increases the slope of the relationship whereas acidosis decreases the slope.

modified from 450
Figure 33. Figure 33.

Relationship between acute changes in plasma pH and potassium secretion (JK) by rat distal tubule. Rats were made acidotic by ammonium chloride gavage and alkalotic by intravenous NaHCO3 infusion.

data from 412
Figure 34. Figure 34.

Effects of acute and chronic metabolic acidosis on urinary potassium excretion.
Figure 35. Figure 35.

Relationship between urinary ammonium and potassium excretion.

modified from 442
Figure 36. Figure 36.

Summary of mechanisms stabilizing potassium balance during water diuresis and antidiuresis. In both conditions, opposing actions of antidiuretic hormone (ADH) and urinary flow rate (tubule flow rate) on potassium secretion by distal tubule (and cortical collecting duct) cancel such that urinary potassium excretion may remain constant and potassium balance is maintained.

from 101,103
Figure 37. Figure 37.

Relationship between steady‐state plasma potassium concentration and potassium excretion as a function of plasm aldosterone in dog. Animals were adrenalectomized and given fixed doses of aldosterone, and potassium content of the diet was varied.

modified from 516
Figure 38. Figure 38.

Relationship between plasma potassium concentration and urinary potassium excretion in dog as a function of dietary sodium intake (in mEq/day). Dogs were adrenalectomized and given a fixed dose of aldosterone, and potassium content of the diet was varied at different sodium intakes.

modified from 513
Figure 39. Figure 39.

Effect of extracellular fluid volume (ECFV) contraction on potassium secretion by distal nephron. Potassium secretion may remain constant because of opposing actions of aldosterone and tubule flow rate on potassium secretion.


Figure 1.

Potassium homeostasis depends on maintenance of external and internal potassium balance. External potassium balance is determined by rate of potassium intake (100 mEq/day) and rate of urinary (90 mEq/day) and fecal excretion (10 mEq/day). Internal potassium balance depends on distribution of potassium between muscle, bone, liver, and red blood cells (RBC) and the extracellular fluid (ECF). This distribution is regulated by several hormones and is affected by acid–base balance and tonicity of plasma. (Movement of potassium between the ECF and cells is indicated by the small arrows; see text for details.)



Figure 2.

Schematic illustration of superficial (right) and juxtamedullary (left) nephrons in mammalian kidney. Arrows indicate direction of potassium transport. Abbreviations: CNT, connecting tubule; DCT, distal convoluted tubule; PCT, proximal convoluted tubule; PST, proximal straight tubule (the entire proximal tubule can also be divided into three segments labeled S1, S2, S3); TAL, thick ascending limb; DTL, descending thin limb; ATL, ascending thin limb; ICT, initial collecting tubule; CCD, cortical collecting duct; TAL, thick ascending limb; OMCDo, outer medullary collecting duct (outer stripe); OMCDi, outer medullary collecting duct (inner stripe); IMCDi, inner medullary collecting duct (initial segments); IMCDt, inner medullary collecting duct (terminal segment).



Figure 3.

Schematic illustration of cell types lining distal tubule and cortical collecting duct in rat. Transitions between distal convoluted tubule (DCT), connecting tubule (CNT), and initial collecting duct (ICT) are gradual in the rat and the human but more abrupt in the rabbit.

from 419


Figure 4.

Koefoed‐Johnson—Ussing cell model of sodium transport across frog skin (modified from 245). As discussed in the text, inclusion of additional potassium transport mechanisms in the apical and/or basolateral membrane can account for potassium transport processes observed along the nephron. Apical solution is electrically negative relative to a grounded bath solution.



Figure 5.

Potassium transport mechanisms in renal cells. Direction and magnitude of potassium transport in each nephron segment is integrally related to distribution of one or more of these mechanisms to apical or basolateral membrane.



Figure 6.

Proximal cell model of potassium transport. Transepithelial voltage is lumen‐negative in early convolutions and lumen‐positive in late convolutions (relative to a grounded bath solution). Potassium conductance of the apical membrane is small relative to the potassium conductance of the basolateral membrane. According to this model, which incorporates all known potassium‐transport mechanisms, transcellular potassium movement can only occur in the secretory direction. As noted in the text, however, potassium is normally absorbed by the proximal tubule. Transcellular potassium absorption requires an active uptake mechanism in the apical membrane (not shown); see text for details.



Figure 7.

Expanded cell model to account for active potassium absorption by proximal tubule. Cellular potassium absorption may be driven by Na+,K+‐ATPase in lateral membranes, which lowers potassium concentration in interspace and provides driving force for potassium diffusion across tight junction from tubular lumen into interspace. Some potassium may then cross basement membrane by solvent drag. Potassium that enters cell via Na+,K+‐ATPase across lateral membrane preferentially diffuses out of cell across basal membrane through potassium channels. For this mechanism to work, potassium diffusion from cell into lateral interspace and from interspace into tubular lumen must be relatively small; see the text for details.

Modified from 478,480


Figure 8.

Model of descending thin limb of Henle's loop illustrating known potassium transport pathways (modified from 281). Potassium transport may either be in the secretory or absorptive direction depending on the orientation of potassium transepithelial concentration gradient.



Figure 9.

Model of cells of thick ascending limb of Henle's loop illustrating known potassium‐transport pathways. Transepithelial voltage is oriented lumen‐positive relative to a grounded bath solution. Cl−− exchanger has been described in apical membrane of mouse thick ascending limb cells 109. This mechanism, in parallel with Na+−H+ exchanger, would mediate electroneutral NaCl absorption 109. Operation of the Cl−− transporter in concert with the Na+−H+ exchanger would reduce or eliminate sodium‐induced changes in intracellular pH.

Modified from 109


Figure 10.

Potassium recycling. Arrows depict route of potassium recycling within renal medulla.



Figure 11.

Cell model of distal convoluted tubule illustrating known potassium‐transport pathways. KCl cotransport mechanism and potassium‐conductive pathway (not shown) mediate potassium secretion across apical membrane. These potassium‐transport pathways are in parallel with a NaCl cotransport mechanism and a sodium conductive pathway. Transepithelial voltage is oriented lumen‐negative relative to a grounded bath solution.



Figure 12.

Model illustrating known potassium‐transport pathways of principal cells in initial and cortical collecting duct.

see text for details


Figure 13.

Current record of potassium channel in apical membrane of principal cells from rabbit cortical collecting duct. Record was obtained in the cell‐attached configuration with 70 mM NaCl and 70 mM KCl (pH 7.4, Ca2+ free) in the bath and 140 mM KCl in the pipette at 37°C. Closed state is indicated by “C,” and clamp voltage is indicated on left side of the figure. Downward deflection is inward current; upward deflection, outward current.

from 468


Figure 14.

Known hormones and elements regulating small‐conductance apical potassium channel, basolateral potassium channels, and apical sodium channels in principal cells of the cortical collecting duct.

Modified from ref. 475


Figure 15.

Model of the acid‐secreting intercalated cell type in the collecting duct illustrating possible mechanisms of potassium absorption. Potassium may be absorbed via a K+,H+‐ATPase located in the apical membrane. This mechanism may be expressed only during potassium depletion. The mechanism of potassium exit from the cell into the blood is unknown. An H+‐ATPase is also present in the apical membrane. It is not known whether H+‐ATPase and H+,K+‐ATPase are both present in control and potassium‐depleted states.



Figure 16.

Model of inner medullary collecting duct cell (initial segment) illustrating potassium transport pathways. Sodium uptake across apical membrane is mediated by amiloride‐sensitive cation channel (Pna/Pk = 1) in initial segment. In terminal segment, apical membrane does not contain significant conductive pathway for sodium. Potassium transport by this segment may be exclusively paracellular, or may occur via cellular pathway. Cellular route requires potassium transport mechanism in apical membrane. Because cation channel is also conductive to potassium, secretion may occur via this pathway when potassium concentration in tubular fluid is low. The Na+−2Cl−−K+ cotransport mechanism in basolateral membrane is present only in rat 147,362.



Figure 17.

Relationship between plasma potassium concentration and potassium secretion by rat distal tubule perfused in vivo at constant flow rate. Potassium was infused intravenously over 4 hours.

from 420


Figure 18.

Effects of potassium (k+), aldosterone (Aldo), k+, and Aldo and dexamethasone (Dex) on potassium secretion (JK; top panel) by distal tubules, urinary potassium excretion (UKV; bottom panel), and urine flow rate (V middle panel).

from 102


Figure 19.

Effect of increased plasma potassium levels on potassium secreting by distal tubule (JK) in control and K‐adapted rats. Potassium‐adapted rats were fed high potassium diet for 2–4 weeks; open bars, plasma potassium 4 mEq/liter: hatched bars, plasma potassium about 7 mEq/liter. Control tubules secreted less potassium than tubules from potassium‐adapted animals. When challenged with an acute K+ load, control animals increased K excretion modestly, although plasma K+ rose to about 7 mEq/liter. In contrast, administration of similar K+ load to K+‐adapted animals led to sharp increase of K+ secretion, although plasma potassium increased less than that in control animals.

Data from 419,420


Figure 20.

Relationship between whole body potassium content as function of plasma potassium levels in adrenalectomized dogs given normal or high aldosterone (5X). Note that for a given amount of exchangeable potassium, a larger fraction of potassium is sequestered inside cells as aldosterone levels increase. [Modified from 469.] At any plasma potassium level, aldosterone reduces total body potassium.



Figure 21.

Time course of “DOCA‐escape” phenomenon. Aldosterone (Aldo) administration increases sodium and fluid absorption by distal tubule and cortical collecting duct (Phase 1), which leads to volume expansion. Sodium “escapes” from sodium retaining effects because of pressure natriuresis (Phase 2);.

from 100


Figure 22.

Transmission electron micrographs illustrating chronic effect of high‐potassium diet on ultrastructure of principal cells in initial and cortical collecting duct. A. Control. B. K+‐adapted animal given a high‐K+ diet for 4 weeks. Bar equals 1 μm (from 419).



Figure 23.

Effects of chronic DOCA treatment (5 mg/day) on electrophysiological and biochemical properties of cortical collecting ducts isolated from adrenal‐intact rabbits. Data in top and middle panels calculated by equivalent circuit analysis. Top: apical membrane sodium () and potassium () current. Middle: apical membrane potassium () and sodium () conductance. Bottom: activity of Na+,K+‐ATPase.

modified from 332


Figure 24.

Effects of chronic (6–10 days) DOCA treatment on transepithelial voltage (Vte) and driving forces for potassium transport across apical (Va−EK) and basolateral (Vbl−EK) membrane of principal cells in isolated rabbit cortical collecting ducts. The negative value of Va−EK for control and DOCA tubules indicates that potassium diffuses out of the cell into the tubule lumen. With regard to Vbl−EK in control tubules, positive value indicates that potassium diffuses out of cell into blood. In DOCA tubules the driving force reverses such that potassium now enters cells from blood through potassium channels in the basolateral membrane.

modified from 372


Figure 25.

Effects of DOCA on the electrophysiological properties of principal cells in the cortical collecting duct from adrenalectomized rabbits. Top: effects of amiloride on DOCA‐induced changes in sodium () and potassium () currents across apical membrane. Bottom: effects of amiloride on DOCA‐induced changes in potassium () and sodium () conductance of apical membrane.

data from 373


Figure 26.

Equivalent circuit diagram illustrating effects of high‐K+ diet on the electrophysiological properties of the cell membranes and the paracellular pathway in adrenalectomized rabbits. INa = sodium current; IK = potassium current; Gtj = conductance of the tight junction; = sodium conductance of the apical membrane, = potassium conductance of the apical membrane; ENa = Nernst equilibrium potential of sodium; EK = Nernst equilibrium potential of potassium; Va = voltage across apical membrane; Vte = transepithelial voltage; Vb = voltage across basolateral membrane; Ki = intracellular potassium activity; Gb = basolateral membrane conductance, IP max = current through Na+,K+‐ATPase. Currents expressed as μA/cm2, conductance as mS‐cm2 and voltage in mV.

data from 320


Figure 27.

Relationship between tubule perfusion rate and tubular fluid‐to‐potassium concentration ratios ([K+] TF/P) in late distal tubule perfused in vivo from control, low K, and K‐adapted rats.

From 287


Figure 28.

A. Relationship between tubule flow rate and potassium secretion (JK) by rat distal tubules as measured by free‐flow micro‐puncture and tubule perfusion. Relationship between flow and secretion is steeper in free‐flow conditions, except when flow is below 1.5 nl/min. B. Relationship between tubule flow rate and sodium absorption (JNa) in rat distal tubules as measured by free‐flow and tubule perfusion. Relationship is steeper in free‐flow conditions because sodium concentration in tubule fluid increased as flow increased whereas the sodium concentration was unchanged in perfusion experiments.

from 287


Figure 29.

Relationship between tubule perfusion rate and potassium secretion () by isolated rabbit cortical collecting ducts. Solid line and filled circles: data from tubules harvested from animals on a control diet. Open line and open circles: data from tubules harvested from animals with elevated aldosterone levels.

data from 95


Figure 30.

Effects of sodium concentration in tubular lumen ([Na]L) on potassium secretion and transepithelial voltage across perfused rat distal tubules (a, b) and isolated perfused rabbit cortical collecting ducts (c, d).

Data from 133,134,135,423


Figure 31.

Transmission electron micrographs of principal cells in cortical collecting duct of rat. A. Control. B. After 6 days of enhanced sodium delivery into the collecting duct produced by furosemide infusion. Note the cell hypertrophy and selective proliferation of basolateral membrane.

from 222


Figure 32.

Relationship between plasma potassium concentration and urinary potassium excretion in dog. Alkalosis increases the slope of the relationship whereas acidosis decreases the slope.

modified from 450


Figure 33.

Relationship between acute changes in plasma pH and potassium secretion (JK) by rat distal tubule. Rats were made acidotic by ammonium chloride gavage and alkalotic by intravenous NaHCO3 infusion.

data from 412


Figure 34.

Effects of acute and chronic metabolic acidosis on urinary potassium excretion.



Figure 35.

Relationship between urinary ammonium and potassium excretion.

modified from 442


Figure 36.

Summary of mechanisms stabilizing potassium balance during water diuresis and antidiuresis. In both conditions, opposing actions of antidiuretic hormone (ADH) and urinary flow rate (tubule flow rate) on potassium secretion by distal tubule (and cortical collecting duct) cancel such that urinary potassium excretion may remain constant and potassium balance is maintained.

from 101,103


Figure 37.

Relationship between steady‐state plasma potassium concentration and potassium excretion as a function of plasm aldosterone in dog. Animals were adrenalectomized and given fixed doses of aldosterone, and potassium content of the diet was varied.

modified from 516


Figure 38.

Relationship between plasma potassium concentration and urinary potassium excretion in dog as a function of dietary sodium intake (in mEq/day). Dogs were adrenalectomized and given a fixed dose of aldosterone, and potassium content of the diet was varied at different sodium intakes.

modified from 513


Figure 39.

Effect of extracellular fluid volume (ECFV) contraction on potassium secretion by distal nephron. Potassium secretion may remain constant because of opposing actions of aldosterone and tubule flow rate on potassium secretion.

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Article Title: Renal Potassium Transport
 

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Bruce A. Stanton, Gerhard H. Giebisch. Renal Potassium Transport. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 813-874. First published in print 1992. doi: 10.1002/cphy.cp080119