Colonic potassium handling

Sørensen, Mads Vaarby; Matos, Joana; Praetorius, Helle A.; Leipziger, Jens

doi:10.1007/s00424-009-0781-9

Cited by 86 publications

(63 citation statements)

References 133 publications

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“…6,11,12 Previous studies revealed the importance of aldosterone for colonic K + adaptation, 3,54 and showed an upregulation of electrogenic Na + and K + transport and mRNA expression of BK channels and ENaC in the distal colon of mice on a high-K + diet. 11,13 Here, we confirmed that a K + diet induced activation of Na + reabsorption and K + secretion in the colon of AS +/+ mice. However, this adaptation of Na + and K + channel activity was completely absent in the colon of AS 2/2 mice.…”

Section: Discussionmentioning

confidence: 98%

“…6,11,12 We placed colonic mucosa from AS +/+ and AS mice ( Figure 7, A and C). However, in response to the 2% K + diet, K + and Na + channel activities rose significantly in the colonic mucosa of the AS +/+ mice only (Figure 7).…”

Section: Regulation Of Electrolyte Transport In the Late Distal Colonmentioning

confidence: 99%

“…The sole luminal exit pathway is the BK channel. 11 ENaC is also expressed in the colon, but there is no clear dependence of colonic K + secretion on ENaC activity. 12,13 Aldosterone regulates the function of the transport and channel proteins mentioned above by direct stimulation of their expression and/or by modulation of their activity due to an altered expression of regulatory proteins.…”

mentioning

confidence: 99%

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Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Todkar

Picard²,

Loffing‐Cueni³

et al. 2015

Journal of the American Society of Nephrology

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Aldosterone-independent mechanisms may contribute to K + homeostasis. We studied aldosterone synthase knockout (AS 2/2 ) mice to define renal control mechanisms of K + homeostasis in complete aldosterone deficiency. AS 2/2 mice were normokalemic and tolerated a physiologic dietary K + load (2% K + , 2 days) without signs of illness, except some degree of polyuria. With supraphysiologic K + intake (5% K + ), AS 2/2 mice decompensated and became hyperkalemic. High-K + diets induced upregulation of the renal outer medullary K + channel in AS 2/2 mice, whereas upregulation of the epithelial sodium channel (ENaC) sufficient to increase the electrochemical driving force for K + excretion was detected only with a 2% K + diet. Phosphorylation of the thiazide-sensitive NaCl cotransporter was consistently lower in AS 2/2 mice than in AS +/+ mice and was downregulated in mice of both genotypes in response to increased K + intake.Inhibition of the angiotensin II type 1 receptor reduced renal creatinine clearance and apical ENaC localization, and caused severe hyperkalemia in AS 2/2 mice. In contrast with the kidney, the distal colon of AS 2/2 mice did not respond to dietary K + loading, as indicated by Ussing-type chamber experiments. Thus, renal adaptation to a physiologic, but not supraphysiologic, K + load can be achieved in aldosterone deficiency by aldosteroneindependent activation of the renal outer medullary K + channel and ENaC, to which angiotensin II may contribute. Enhanced urinary flow and reduced activity of the thiazide-sensitive NaCl cotransporter may support renal adaptation by activation of flow-dependent K + secretion and increased intratubular availability of Na + that can be reabsorbed in exchange for K + secreted.

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Section: Discussionmentioning

confidence: 98%

Section: Regulation Of Electrolyte Transport In the Late Distal Colonmentioning

confidence: 99%

mentioning

confidence: 99%

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Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Todkar

Picard²,

Loffing‐Cueni³

et al. 2015

Journal of the American Society of Nephrology

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“…30 Although systemic PHA-1 is normally also characterized by hyperkalemia, we did not find a shift in the potassium balance in the Scnn1a KO mice (Figures 4 and 5), which may be explained by differentially regulated and spatially separated electrogenic sodium absorption and potassium secretion. 31 …”

Section: Scnn1amentioning

confidence: 99%

Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance

Malsure

Wang

Charles

et al. 2014

Journal of the American Society of Nephrology

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Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Here, we investigated the importance of ENaC and its positive regulator channel-activating protease 1 (CAP1/Prss8) in colon. Mice lacking the aENaC subunit in colonic superficial cells (Scnn1a KO ) were viable, without fetal or perinatal lethality. Control mice fed a regular or low-salt diet had a significantly higher amiloride-sensitive rectal potential difference (ΔPD amil ) than control mice fed a high-salt diet. In Scnn1a KO mice, however, this salt restriction-induced increase in ΔPD amil did not occur, and the circadian rhythm of ΔPD amil was blunted. Plasma and urinary sodium and potassium did not change with regular or high-salt diets or potassium loading in control or Scnn1a KO mice. However, Scnn1a KO mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Mice lacking the CAP1/Prss8 in colonic superficial cells (Prss8 KO ) were viable, without fetal or perinatal lethality. Compared with controls, Prss8 KO mice fed regular or low-salt diets exhibited significantly reduced ΔPD amil in the afternoon, but the circadian rhythm was maintained. Prss8 KO mice fed a low-salt diet also exhibited sodium loss through feces and higher plasma aldosterone levels. Thus, we identified CAP1/Prss8 as an in vivo regulator of ENaC in colon. We conclude that, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compensated for the absence of ENaC in colonic surface epithelium, leading to colon-specific pseudohypoaldosteronism type 1 with mineralocorticoid resistance without evidence of impaired potassium balance.

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“…BK channels have been implicated in a variety of physiological processes (Berkefeld et al 2010), which range from regulation of smooth muscle tone (Brayden and Nelson 1992) to modulation of hormone and neurotransmitter release (Waring and Turgeon 2009). Interestingly, BK channels are also involved in modulating K + transport in the mammalian kidney (Bailey et al 2006, Pulznick and Sansom 2006, Wang and Giebisch 2009, Holtzclaw et al 2010 and colon epithelium (Sorensen et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Application of a real-time PCR assay to detect BK potassium channel expression in samples from Atlantic salmon (Salmo salar) and Rainbow trout (Oncorhynchus mykiss) acclimated to freshwater#

et al. 2015

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Colonic potassium handling

Cited by 86 publications

References 133 publications

Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Mechanisms of Renal Control of Potassium Homeostasis in Complete Aldosterone Deficiency

Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance

Application of a real-time PCR assay to detect BK potassium channel expression in samples from Atlantic salmon (Salmo salar) and Rainbow trout (Oncorhynchus mykiss) acclimated to freshwater#

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