Renal Chloride Channels in Relation to Sodium Chloride Transport

Teulon, Jacques; Planelles, Gabrielle; Sepúlveda, Francisco V.; Andrini, Olga; Lourdel, Stéphane; Paulais, Marc

doi:10.1002/cphy.c180024

Cited by 14 publications

(10 citation statements)

References 433 publications

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“…The increase of urinary excretion of chloride can be attributed to the renal mechanisms responsible for its reabsorption. Renal reabsorption of this electrolyte is dependent of the electrochemical gradient generated by the presence of sodium reabsorbed into the peritubular space (25). In the present work, the urinary excretion of sodium and chloride varied similarly in both treatments over time.…”

Section: Discussionsupporting

confidence: 49%

Effects of Hypotonic and Isotonic Enteral Electrolyte Solutions Administered in Continuous Flow in Weaned Foals

et al. 2020

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The effects of fluid therapy with maintenance enteral electrolytic solutions administered by nasogastric route in continuous flow have not previously been studied in weaned foals. This study primary goal was to compare the effects of two maintenance enteral electrolytic solutions administered by nasogastric route in continuous flow on the hydro electrolytic balance in weaned foals. This paper was a controlled trial in a cross-over design (6 × 2) performed in six foals with a mean age of 7.3 ± 1.4 months; each animal received two treatments, IsoES and HypoES, with an interval of 7 days between treatments. After 12 h of fasting, the animals were treated with enteral electrolyte solutions administered via nasogastric route in continuous flow in a volume of 15 mL/kg/h for 12 h. The evaluations were performed at T-12h (the beginning of the fasting), T0h (end of fasting and beginning of fluid therapy), T4h (4 h of fluid therapy), T8h (8 h of fluid therapy), T12h (end of fluid therapy), and T24h (12 h after the end of fluid therapy). Twelve hours of fasting resulted in a reduction (P < 0.05) in body weight, abdominal circumference, whereas serum sodium, SID and enophthalmos increased. Twelve hours of fluid therapy normalized these parameters and promoted increased urinary volume and decreased urinary density without causing electrolyte imbalances. Both enteral electrolytic solutions were effective in reestablishing clinical and laboratorial variables without causing electrolyte imbalances.

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Section: Discussionsupporting

confidence: 49%

Effects of Hypotonic and Isotonic Enteral Electrolyte Solutions Administered in Continuous Flow in Weaned Foals

et al. 2020

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“…In the proximal tubule chloride is mainly reabsorbed paracellularly in the S3 segment. Therefore, a shift of solute transport from the S1/S2 segments to the S3 segment could explain the increase in plasma chloride [23]. Effects of dapagliflozin on transcellular chloride transport seem less likely, as these are coupled to bicarbonate, and we found no effects on plasma bicarbonate [24].…”

Section: Discussionmentioning

confidence: 51%

SGLT2 inhibition versus sulfonylurea treatment effects on electrolyte and acid–base balance: secondary analysis of a clinical trial reaching glycemic equipoise: Tubular effects of SGLT2 inhibition in Type 2 diabetes

et al. 2020

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Sodium–glucose transporter (SGLT)2 inhibitors increase plasma magnesium and plasma phosphate and may cause ketoacidosis, but the contribution of improved glycemic control to these observations as well as effects on other electrolytes and acid–base parameters remain unknown. Therefore, our objective was to compare the effects of SGLT2 inhibitors dapagliflozin and sulfonylurea gliclazide on plasma electrolytes, urinary electrolyte excretion, and acid–base balance in people with Type 2 diabetes (T2D). We assessed the effects of dapagliflozin and gliclazide treatment on plasma electrolytes and bicarbonate, 24-hour urinary pH and excretions of electrolytes, ammonium, citrate, and sulfate in 44 metformin-treated people with T2D and preserved kidney function. Compared with gliclazide, dapagliflozin increased plasma chloride by 1.4 mmol/l (95% CI 0.4–2.4), plasma magnesium by 0.03 mmol/l (95% CI 0.01–0.06), and plasma sulfate by 0.02 mmol/l (95% CI 0.01–0.04). Compared with baseline, dapagliflozin also significantly increased plasma phosphate, but the same trend was observed with gliclazide. From baseline to week 12, dapagliflozin increased the urinary excretion of citrate by 0.93 ± 1.72 mmol/day, acetoacetate by 48 μmol/day (IQR 17–138), and β-hydroxybutyrate by 59 μmol/day (IQR 0–336), without disturbing acid–base balance. In conclusion, dapagliflozin increases plasma magnesium, chloride, and sulfate compared with gliclazide, while reaching similar glucose-lowering in people with T2D. Dapagliflozin also increases urinary ketone excretion without changing acid–base balance. Therefore, the increase in urinary citrate excretion by dapagliflozin may reflect an effect on cellular metabolism including the tricarboxylic acid cycle. This potentially contributes to kidney protection.

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“…In parallel, Clc-Kb/2 channels, together with the β-subunit barttin, allow chloride exit across the basolateral membrane [64,65] (Figure 1). This provides a potential mechanism to link changes in extracellular potassium to changes in intracellular chloride.…”

Section: Role Of Basolateral Potassium and Chloride Channels In The Dctmentioning

confidence: 99%

Intracellular chloride

Rodan

2019

Current Opinion in Nephrology and Hypertension

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Purpose of review-This review focuses on the role of intracellular chloride in regulating transepithelial ion transport in the distal convoluted tubule (DCT) in response to perturbations in plasma homeostasis. Recent findings-Low dietary potassium increases the phosphorylation and activity of the sodium chloride cotransporter (NCC) in the DCT, and vice versa, affecting sodium-dependent potassium secretion in the downstream aldosterone-sensitive distal nephron. In cells, NCC phosphorylation is increased by lowering of intracellular chloride, via activation of the chloridesensitive WNK (With No Lysine)-SPAK/OSR1 (Ste20-related proline/alanine rich kinase/ oxidative stress response) kinase cascade. In vivo studies have demonstrated pathway activation in the kidney in response to low dietary potassium. A possible mechanism is lowering of DCT intracellular chloride in response to low potassium due to parallel basolateral potassium and chloride channels. Recent studies support a role for these channels in the response of NCC to varying potassium. Studies examining chloride-insensitive WNK mutants, in the Drosophila renal tubule and in the mouse, lend further support to a role for chloride in regulating WNK activity and transepithelial ion transport. Caveats, alternatives and future directions are also discussed. Summary-Chloride sensing by WNK kinase provides a mechanism to allow coupling of extracellular potassium with NCC phosphorylation and activity to maintain potassium homeostasis.

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Renal Chloride Channels in Relation to Sodium Chloride Transport

Cited by 14 publications

References 433 publications

Effects of Hypotonic and Isotonic Enteral Electrolyte Solutions Administered in Continuous Flow in Weaned Foals

Effects of Hypotonic and Isotonic Enteral Electrolyte Solutions Administered in Continuous Flow in Weaned Foals

SGLT2 inhibition versus sulfonylurea treatment effects on electrolyte and acid–base balance: secondary analysis of a clinical trial reaching glycemic equipoise: Tubular effects of SGLT2 inhibition in Type 2 diabetes

Intracellular chloride

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