Evidence for gut factor in K<sup>+</sup> homeostasis

Lee, Felix N.; Oh, Gisuk; McDonough, Alicia A.; Youn, Jang H.

doi:10.1152/ajprenal.00427.2006

Cited by 52 publications

(66 citation statements)

References 24 publications

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“…The tray was replaced every hour to collect urine passed. To obtain a constant flow of urine, animals were infused with a constant volume (4.1 ml/h) of fluid (saline or saline ϩ KCl during K ϩ infusion) throughout the experiment (15). This infusion volume did not appear to affect K ϩ excretion, as the baseline K ϩ excretion rate was indistinguishable from the basal rate of K ϩ excretion measured in fasting rats without fluid infusion between 7 AM and 7 PM (data not shown).…”

Section: Animalsmentioning

confidence: 95%

“…Feedforward control of K ϩ homeostasis was supported by our recent study (15) that examine the effects of K ϩ infusion into stomach vs. hepatic portal vein or a systemic vein on plasma [K ϩ ] and renal K ϩ excretion in rats. Our results indicated that the K ϩ infusions via these different routes resulted in similar profiles of plasma [K ϩ ] and renal K ϩ excretion in fasting states.…”

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confidence: 94%

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Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Kim

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Dietary K+ intake may increase renal K+ excretion via increasing plasma [K+] and/or activating a mechanism independent of plasma [K+]. We evaluated these mechanisms during normal dietary K+ intake. After an overnight fast, [K+] and renal K+ excretion were measured in rats fed either 0% K+ or the normal 1% K+ diet. In a third group, rats were fed with the 0% K+ diet, and KCl was infused to match plasma [K+] profile to that of the 1% K+ diet group. The 1% K+ feeding significantly increased renal K+ excretion, associated with slight increases in plasma [K+], whereas the 0% K+ diet decreased K+ excretion, associated with decreases in plasma [K+]. In the KCl-infused 0% K+ diet group, renal K+ excretion was significantly less than that of the 1% K+ group, despite matched plasma [K+] profiles. We also examined whether dietary K+ alters plasma profiles of gut peptides, such as guanylin, uroguanylin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide, pituitary peptides, such as AVP, α-MSH, and γ-MSH, or aldosterone. Our data do not support a role for these hormones in the stimulation of renal K+ excretion during normal K+ intake. In conclusion, postprandial increases in renal K+ excretion cannot be fully accounted for by changes in plasma [K+] and that gut sensing of dietary K+ is an important component of the regulation of renal K+ excretion. Our studies on gut and pituitary peptide hormones suggest that there may be previously unknown humoral factors that stimulate renal K+ excretion during dietary K+ intake.

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Section: Animalsmentioning

confidence: 95%

mentioning

confidence: 94%

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Kim

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…14 argued that the increase in serum potassium after a high-potassium meal is too small (0.5 mEq/L) to initiate either of these adaptive responses and that an intestinal signal is responsible for the increase in renal potassium excretion after a high potassium meal. Recent, interesting work from Lee et al 13 further strengthened this observation. Lee et al showed that the administration of potassium by intravenous, intraportal, or intragastric method has a similar effect on plasma potassium and renal potassium excretion profiles in the fasting state but that the administration of a low-potassium meal along with intragastric potassium infusion substantially reduces the increase in plasma potassium and greatly enhances renal potassium excretion.…”

Section: Enteric Modulation Of Renal Sodium and Potassiummentioning

confidence: 79%

“…Elevated serum potassium directly alters potassium excretion by collecting duct cells and thereby promotes kaliuresis. [11][12][13] An elevation in serum potassium concentration also increases aldosterone synthesis, which, in turn, increases kaliuresis. 14 argued that the increase in serum potassium after a high-potassium meal is too small (0.5 mEq/L) to initiate either of these adaptive responses and that an intestinal signal is responsible for the increase in renal potassium excretion after a high potassium meal.…”

Section: Enteric Modulation Of Renal Sodium and Potassiummentioning

confidence: 99%

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Control of Renal Solute Excretion by Enteric Signals and Mediators

Thomas

Kumar

2008

Journal of the American Society of Nephrology

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The renal response to ingested solutes and the regulation of nutrient and solute balance are vital for the well-being of an organism. Foods that contain protein, carbohydrate, and fat are processed to amino acids, monosaccharides, and fatty acids and triglycerides. These substances and electrolytes and minerals are absorbed with varying degrees of efficiency in the intestine, often in response to the perceived needs of the organism. In some instances, the amount of the nutrient absorbed in the intestine depends on the amount present in the diet, and with large influxes of nutrient materials into the extracellular fluid, it falls to the kidney to remove the excessive amounts absorbed by the intestine from the serum and extracellular fluid, either by increasing the amount excreted by tubular processes or by reducing the amount reabsorbed in the tubule after glomerular filtration.It is widely believed that the renal response to ingested solutes is regulated by hormones such as aldosterone, in the case of sodium and potassium, and parathyroid hormone and the vitamin D endocrine system, in the case of calcium and phosphate. New (and old) information also suggests that factors produced in the gastrointestinal tract are released after changes in intestinal luminal solute concentrations and mediate changes in renal solute transport. This "enteric-renal solute-transporting regulating axis" represents an underappreciated mechanism by which renal solute transport is regulated. ENTERIC MODULATION OF RENAL SODIUM AND POTASSIUMDietary sodium induces a more marked natriuresis than intravenous sodium. The regulation of renal excretory or reabsorptive processes exclusively depends on the activity of various hormones or local renal factors, the synthesis or release of which depends on alterations in the serum or extracellular fluid concentrations of the various ions. Decreases in renal sodium excretion in response to a low-salt diet depend on changes in aldosterone synthesis. 1 Indeed, a lack of aldosterone synthesis is responsible for many of the manifestations of Addison's disease. The role of aldosterone (and inhibition of its synthesis) in increasing salt excretion is less clearly defined when a high-salt diet is ingested. Data suggest that other factors play a role in this process and that the role of aldosterone is minimal in the adaptation to high-sodium meals. Carey and others 2-4 have demonstrated that salt-depleted individuals who were given oral sodium chloride excreted much more sodium in their urine than did individuals who were given the same amount of sodium chloride intravenously. Plasma aldosterone ABSTRACTRenal solute excretion is important for the homeostasis of various ions. It is widely believed that hormones such as aldosterone, parathyroid hormone, the vitamin D endocrine system, and growth factors are responsible for alterations in renal ion transport in response to increased absorption of enteric solutes. In the cases of sodium, potassium, and phosphorus, moieties produced in the gastrointestinal tract a...

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Renal Ammonia Metabolism and Transport

Weiner

Verlander

2013

Comprehensive Physiology

171

136

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Renal ammonia metabolism and transport mediates a central role in acid-base homeostasis. In contrast to most renal solutes, the majority of renal ammonia excretion derives from intrarenal production, not from glomerular filtration. Renal ammoniagenesis predominantly results from glutamine metabolism, which produces 2 NH4+ and 2 HCO3− for each glutamine metabolized. The proximal tubule is the primary site for ammoniagenesis, but there is evidence for ammoniagenesis by most renal epithelial cells. Ammonia produced in the kidney is either excreted into the urine or returned to the systemic circulation through the renal veins. Ammonia excreted in the urine promotes acid excretion; ammonia returned to the systemic circulation is metabolized in the liver in a HCO3−-consuming process, resulting in no net benefit to acid-base homeostasis. Highly regulated ammonia transport by renal epithelial cells determines the proportion of ammonia excreted in the urine versus returned to the systemic circulation. The traditional paradigm of ammonia transport involving passive NH3 diffusion, protonation in the lumen and NH4+ trapping due to an inability to cross plasma membranes is being replaced by the recognition of limited plasma membrane NH3 permeability in combination with the presence of specific NH3-transporting and NH4+-transporting proteins in specific renal epithelial cells. Ammonia production and transport are regulated by a variety of factors, including extracellular pH and K+, and by several hormones, such as mineralocorticoids, glucocorticoids and angiotensin II. This coordinated process of regulated ammonia production and transport is critical for the effective maintenance of acid-base homeostasis.

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Evidence for gut factor in K⁺ homeostasis

Cited by 52 publications

References 24 publications

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Control of Renal Solute Excretion by Enteric Signals and Mediators

Renal Ammonia Metabolism and Transport

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Evidence for gut factor in K+ homeostasis

Cited by 52 publications

References 24 publications

Gut sensing of dietary K+ intake increases renal K+ excretion

Gut sensing of dietary K+ intake increases renal K+ excretion

Control of Renal Solute Excretion by Enteric Signals and Mediators

Renal Ammonia Metabolism and Transport

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Evidence for gut factor in K⁺ homeostasis

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion

Gut sensing of dietary K⁺ intake increases renal K⁺ excretion