Sodium Chloride Coupled Transport in Mammalian Nephrons

Burg, Maurice B.; Good, David W.

doi:10.1146/annurev.ph.45.030183.002533

Cited by 45 publications

(25 citation statements)

References 49 publications

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“…This is compatible with a (Na+-K+-2Cl-) co-transport system which would transport 36 mol ofelectrolyte per mol of02 whereas an (Na+-Cl-) co-transport system would transport a maximum of 18 mol. This conclusion is also consistent with recent findings in other epithelia where (Na+-K+-2Cl-) co-transport seems to be involved (see Burg & Good, 1983 (Young & Ellory, 1977), unlike carnivore red cells (Ellory, Jones, Preston & Young, 1982). We have measured glutamine uptake in human red cells as a possible glutamate source for glutathione biosynthesis.…”

Section: Psupporting

confidence: 92%

Proceedings of the Physiological Society, 11‐12 November 1983, Queen Elizabeth College, London Meeting: Communications

1984

The Journal of Physiology

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Section: Psupporting

confidence: 92%

Proceedings of the Physiological Society, 11‐12 November 1983, Queen Elizabeth College, London Meeting: Communications

1984

The Journal of Physiology

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“…At high tubule flow rates, this transepithelial electrical potential averages 3-10 mV, lumen-positive. 65 At low flow rates, this voltage is augmented by a superimposed NaCl dilution potential. This is caused by the generation of a NaCl concentration gradient (tubule lower than interstitium) across the epithelium, which has a Na + to Cl 2 permeability ratio (P Na /P Cl ) of 2-6, [66][67][68] presumably reflecting a cation-selective paracellular shunt.…”

Section: Role Of Claudins In the Thick Ascending Limbmentioning

confidence: 99%

Claudins and the Kidney

2015

Journal of the American Society of Nephrology

121

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Claudins are tight-junction membrane proteins that function as both pores and barriers in the paracellular pathway in epithelial cells. In the kidney, claudins determine the permeability and selectivity of different nephron segments along the renal tubule. In the proximal tubule, claudins have a role in the bulk reabsorption of salt and water. In the thick ascending limb, claudins are important for the reabsorption of calcium and magnesium and are tightly regulated by the calcium-sensing receptor. In the distal nephron, claudins need to form cation barriers and chloride pores to facilitate electrogenic sodium reabsorption and potassium and acid secretion. Aldosterone and the with-no-lysine (WNK) proteins likely regulate claudins to fine-tune distal nephron salt transport. Genetic mutations in claudin-16 and -19 cause familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphisms in claudin-14 are associated with kidney stone risk. It is likely that additional roles for claudins in the pathogenesis of other types of kidney diseases have yet to be uncovered.

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“…Thick ascending limbs reabsorb about 30% of the filtered load of NaCl 1, 2 . About 50–70% of the Na traverses the transcellular pathway, entering the cell via Na/K/2Cl cotransport and Na/H exchange, and exiting via Na/K ATPase.…”

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Nitric Oxide Decreases the Permselectivity of the Paracellular Pathway in Thick Ascending Limbs

Monzón

Garvin

2015

Hypertension

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Thick ascending limbs (THALs) reabsorb 25–30% of the filtered NaCl. About 50–70% is reabsorbed via the transcellular pathway and 30–50% is reabsorbed through the Na-selective paracellular pathway. Nitric oxide (NO) inhibits transepithelial Na reabsorption, but its effects on the paracellular pathway are unknown. We hypothesized that NO decreases the selectivity of the paracellular pathway in THALs via cGMP-dependent protein kinase (PKG). To assess relative Na/Cl permeability ratios (PNa/PCl), we perfused rat THALs and measured the effect of reducing bath NaCl on transepithelial voltage, creating dilution potentials, with vehicle, NO donors and endogenous NO. PNa/PCl was calculated using the Goldman-Hodgkin-Katz equation. Reducing bath Na/Cl to 16/8; 32/24; and 64/56 mmol/l created dilution potentials of −13.6 ± 2.2, −10.8 ± 3.0, and −6.1 ± 0.9 mV, respectively. Calculated PNa/PCls were 2.0 ± 0.2, 2.2 ± 0.5, and 1.9 ± 0.2. The NO donor spermine NONOate (SPM; 200 μmol/l) blunted the dilution potential caused by 32/24 mmol/l Na/Cl from −11.1 ± 2.1 to −6.5 ± 1.6 mV (p<0.004) and PNa/PCl from 2.2 ± 0.4 to 1.5± 0.2. Nitroglycerin (200 μmol/l), another NO donor, also reduced PNa/PCl. Controls showed no significant changes. Dibutyryl-cGMP decreased dilution potentials from −13.4 ± 2.9 to −7.5 ± 1.8 mV (n=6, p<0.01). PKG inhibition with KT5823 (4μM) blocked the effect of SPM, while phosphodiesterase 2 inhibition did not. Endogenously-produced NO mimicked the effect of the NO donors. Conclusion: NO reduces the selectivity of the paracellular pathway in thick ascending limbs via cGMP and PKG.

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Sodium Chloride Coupled Transport in Mammalian Nephrons

Cited by 45 publications

References 49 publications

Proceedings of the Physiological Society, 11‐12 November 1983, Queen Elizabeth College, London Meeting: Communications

Proceedings of the Physiological Society, 11‐12 November 1983, Queen Elizabeth College, London Meeting: Communications

Claudins and the Kidney

Nitric Oxide Decreases the Permselectivity of the Paracellular Pathway in Thick Ascending Limbs

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