Renal Energy Metabolism and Sodium Reabsorption

Lewy, Peter; Quintanilla, A.; Levin, Nathan W.; Kessler, R H

doi:10.1146/annurev.me.24.020173.002053

Cited by 29 publications

(24 citation statements)

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“…Both the electrical potential and net water flux fell to zero in the presence of 1 mM iodoacetate, an inhibitor of glycolysis (20); however, potassium cyanide (1 mM), an inhibitor of ATP generation by mitochondrial electron transport in aerobic metabolism (21), had no effect on the electrical potential. The MDCK cells in culture are in this respect very similar to the anaerobically adapted fresh water turtle, which is highly resistant to cyanide (22) and can maintain sodium transport across the urinary bladder during anaerobiosis and cyanide exposure (23).…”

Section: Discussionmentioning

confidence: 99%

Transepithelial transport in cell culture.

Misfeldt¹,

Hamamoto²,

Pitelka³

1976

Proc. Natl. Acad. Sci. U.S.A.

455

247

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In cell culture a kidney epithelial cell line, MDCK, forms a continuous sheet of identically oriented asymmetrical cells joined by circumferential occluding junctions. The reconstructed epithelial membrane has transport and permeability qualities of in vivo transporting epithelia.The cell layer can e readily manipulated when cultured on a freely permeable membrane filter and, when placed in an Ussing chamber, electrophysiological measurements can be taken. In the absence of a chemical gradient, the cell layer generates an electrical potential of 1.42 mV, the apical surface negative. It is an effective permeability barrier and lacks significant shunting at the clamped edge, as indicated by a resistance of 84 ohms.cm2, which increased when bulk flow from basolateral to apical was induced by an osmotic gradient or electroosmosis. The MDCK cell layer is cation selective with a relative permeability ratio, PNa/PCI, of 1.7. Net water flux, apical to basolateral, was 7.3 Ml cm2 hr'1 in the absence of a chemical gradient. The morphological and functional qualities of a transporting epithelium are stable in cell culture, and the potentia use of a homogeneous cell nopulation in cell culture would enhance studies of epithelial transport at the cellular and subcellular levels. In 1969 Leighton et al. (1) and Auersperg (2) described the occurrence of domes, turgid, fluid-filled, blister-like hemicysts, in cell cultures of renal and uterine cervix epithelia, respectively. Subsequently, domes have been reported in cell cultures of normal (3) and. neoplastic (4) mouse mammary epithelia, mouse liver (5), human breast adenocarcinoma (6), pig kidney (7), and frog urinary bladder epithelium (unpublished observation). In each instance, the cells cultured were from transporting epithelia. That domes represent a transport phenomenon is suggested by the presence of morpho--logical polarity unique to transporting epithelia (8), apical microvilli extending upward into the medium and occluding junctions joining adjacent cells at the apical-basolateral membrane border. As well, time-lapse photography revealed domes to be localized regions of the cell layer that lift off the culture dish substratum, gradually expand to a maximum, and then rapidly collapse (9). The establishment and characterization of epithelial transport function in cell culture has both experimental and biological significance. The cells were cultured in Waymouth's 752/1 medium (GIBCO) supplemented with penicillin (100 units/ml), streptomycin (100,gg/ml), insulin (26 IU/ml) (11), and 10% (vol/vol) fetal calf serum. Experiments were performed on cultures 4-21 days after plating. Membrane filters, 25 mm (Millipore HAMK 02512), were boiled for 5-10 min to remove the wetting agent and sterilize. The wet filters were affixed to plastic culture dishes by droplets of Millipore Cement Formulation no. 1 applied around the edge to hold the filter flat. The cultured cells were plated directly into the culture dish over the filter. When the cell layer and underlying filter w...

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Section: Discussionmentioning

confidence: 99%

Transepithelial transport in cell culture.

Misfeldt¹,

Hamamoto²,

Pitelka³

1976

Proc. Natl. Acad. Sci. U.S.A.

455

247

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“…Proximal tubules utilize non- esterified fatty acids, such as palmitate, via β-oxidation for maximal ATP production. A single molecule of palmitate produces 106 molecules of ATP, whereas the oxidation of glucose only yields 36 molecules of ATP 17,18 . Fatty acids are taken up by proximal tubule cells via transport proteins, such as platelet glycoprotein 4 (also known as CD36), or synthesized in the cytoplasm, where they are activated by coA before being transported into mitochondria through the 19 (FIG.…”

Section: Mitochondrial Functionmentioning

confidence: 99%

Mitochondrial energetics in the kidney

2017

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The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.

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“…The intact mammalian kidney reabsorbs nearly 80 meq Na/g kidney/day across the renal tubules and accounts for nearly 70% of oxygen utilization by the kidney (306). To meet this demand, tubule cells generate a significant amount of ATP.…”

Section: Cellular Response To Injurymentioning

confidence: 99%

Pathophysiology of Acute Kidney Injury

Basile

Anderson

Sutton

2012

Comprehensive Physiology

936

906

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Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.

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Renal Energy Metabolism and Sodium Reabsorption

Cited by 29 publications

References 0 publications

Transepithelial transport in cell culture.

Transepithelial transport in cell culture.

Mitochondrial energetics in the kidney

Pathophysiology of Acute Kidney Injury

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