scholarly journals Regulation of erythropoietin production is related to proximal tubular function

1989 ◽  
Vol 256 (5) ◽  
pp. F942-F947 ◽  
Author(s):  
K. U. Eckardt ◽  
A. Kurtz ◽  
C. Bauer
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Sensor ◽  
Collecting Duct ◽  
Inhibitory Effect ◽  
Tubular Function ◽  
Sodium Reabsorption ◽  
Renal Oxygen Consumption ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Renal Oxygen

Regulation of renal erythropoietin (EPO) production is based on an intrarenal oxygen sensor. Whereas the sensitivity of this oxygen sensor to variations in renal oxygen supply is well established, the influence of changes in renal oxygen consumption has not yet been elucidated. Diuretic drugs, which inhibit active sodium reabsorption, reduce tubular oxygen consumption. We therefore investigated the effects of acetazolamide, furosemide, hydrochlorothiazide, and amiloride, known to preferentially inhibit sodium reabsorption at different segments of the nephron, on hypoxia-induced EPO formation in mice. Those drugs that are considered to act mainly in the loop of Henle, distal tubule, and collecting duct (furosemide, hydrochlorothiazide, and amiloride) did not impair EPO formation. Acetazolamide on the other hand, which is thought to act predominantly at the proximal tubular site, significantly reduced EPO formation in response to normobaric hypoxia (8 and 14% O2) and functional anemia (0.1% carbon monoxide). This inhibitory effect of acetazolamide was dose dependent and correlated with the natriuresis induced. It appeared not to depend on the metabolic acidosis induced by the drug, since the simultaneous administration of sodium bicarbonate, which restored standard bicarbonate levels to normal, did not diminish the inhibitory effect of acetazolamide on EPO production. In conclusion the data suggest that the regulation of EPO production is likely to be related to proximal tubular function.

Proximal tubular Na, Cl, and HCO3 reabsorption and renal oxygen consumption

1984 ◽  
Vol 247 (1) ◽  
pp. F151-F157 ◽  
Author(s):  
S. W. Weinstein ◽  
R. Klose ◽  
J. Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Ion Transport ◽  
Rat Kidney ◽  
Fluid Reabsorption ◽  
Bicarbonate Reabsorption ◽  
Renal Oxygen Consumption ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption ◽  
Renal Oxygen

The majority of the oxygen consumed by the rat kidney appears to occur in the proximal tubule. Therefore changes in metabolically linked ion transport in this segment of the nephron should result in changes in renal oxygen consumption. To study the role of bicarbonate reabsorption in metabolically linked proximal tubular ion transport a series of micropuncture-clearance-extraction experiments were performed comparing the effects of the carbonic anhydrase inhibitor benzolamide and of hypertonic sodium bicarbonate infusion with control conditions in the rat. End-proximal tubular fluid and chloride reabsorption were measured. From these, the rates of sodium and bicarbonate reabsorption were estimated. Simultaneously with the tubular fluids, extraction collections were obtained for determination of renal oxygen consumption. Both benzolamide and hypertonic bicarbonate reduced proximal tubular fluid reabsorption while concomitantly reducing the transepithelial gradient for chloride. The mean rate of renal oxygen consumption did not differ from the control rate in either experimental group and could be dissociated from the calculated net rates of proximal tubular sodium, chloride, and bicarbonate reabsorption. We interpret these data as evidence that proximal tubular hydrogen ion secretion supporting bicarbonate reabsorption requires at most small amounts of oxidative energy, less than detectable by these techniques. The data, in contrast, support the conclusion that the chloride-bicarbonate transepithelial gradient appears to be an important passive driving force in vivo for proximal tubular fluid reabsorption.

Renal sodium transport and oxygen consumption

1961 ◽  
Vol 201 (3) ◽  
pp. 511-516 ◽  
Author(s):  
Fredrik Kiil ◽  
Knut Aukland ◽  
Harald E. Refsum
Keyword(s):  
Oxygen Consumption ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Transport ◽  
Filtration Rate ◽  
Sodium Reabsorption ◽  
Renal Oxygen Consumption ◽  
Tubular Lumen ◽  
Oxygen Difference ◽  
Renal Oxygen

Glomerular filtration rate and renal blood flow were increased in dogs by infusion of 2% glycine and hypertonic NaCl at rates of 8 ml/min. This procedure resulted both in an increased rate of sodium reabsorption and in increased oxygen consumption. Approximately six equivalents of sodium were transported per equivalent oxygen consumed, a ratio similar to that obtained by others when glomerular filtration rate had been reduced. These observations strongly suggest that a large part of renal oxygen consumption is related to the transport of sodium. When the rate of sodium reabsorption was reduced during mannitol diuresis, arteriovenous oxygen difference decreased, but renal oxygen consumption remained unchanged. It is suggested that the active sodium transport in the proximal tubules continues at an unchanged rate during mannitol diuresis but that net reabsorption is reduced owing to increased passive influx into the tubular lumen when the transtubular concentration gradient increases. Other interpretations are discussed.

Energetics of tubular sodium reabsorption sensitive to ethacrynic acid and ouabain

1982 ◽  
Vol 242 (3) ◽  
pp. F254-F260 ◽  
Author(s):  
O. M. Sejersted ◽  
P. A. Steen ◽  
F. Kiil
Keyword(s):  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Cell Membrane ◽  
Ethacrynic Acid ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Renal Oxygen Consumption ◽  
Anesthetized Dogs ◽  
Futile Cycling ◽  
Renal Oxygen

Ouabain reduces renal oxygen consumption more extensively than ethacrynic acid despite similar natriuretic effects. Therefore, ethacrynic acid, which does not inhibit Na-K-ATPase, might stimulate energy metabolism unrelated to net sodium reabsorption. Experiments were performed on anesthetized dogs that had received isotonic saline intravenously corresponding to 10% of body wt and acetazolamide (100 mg.kg-1 i.v.). Subsequent infusion of ouabain in nine dogs (120 nmol.kg-1 intrarenally) reduced sodium reabsorption and oxygen consumption in parallel, giving a delta Na/delta O2 ratio of 18.0 +/- 1.1. With ethacrynic acid (3 mg.kg-1 i.v.) in six other dogs the delta Na/delta O2 ratio averaged 24.5 +/- 1.4. In a third group of five dogs, ouabain administered after ethacrynic acid reduced sodium reabsorption and oxygen consumption to the same levels as when ouabain was given alone. Thus, the high oxygen consumption remaining after ethacrynic acid can be inhibited by ouabain. We propose that ethacrynic acid generates a futile cycling of sodium by Na-K-ATPase across the basolateral cell membrane that is not apparent as net sodium reabsorption and is stopped by ouabain.U

Evidence that renal arterial-venous oxygen shunting contributes to dynamic regulation of renal oxygenation

2007 ◽  
Vol 292 (6) ◽  
pp. F1726-F1733 ◽  
Author(s):  
Chai-Ling Leong ◽  
Warwick P. Anderson ◽  
Paul M. O'Connor ◽  
Roger G. Evans
Keyword(s):  
Oxygen Consumption ◽  
Renal Cortex ◽  
Oxygen Metabolism ◽  
Renal Tissue ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Arterial Infusion ◽  
Dynamic Regulation ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

Renal blood flow (RBF) can be reduced in rats and rabbits by up to 40% without significant changes in renal tissue Po2. We determined whether this occurs because renal oxygen consumption changes with RBF or due to some other mechanism. The relationships between RBF and renal cortical and medullary tissue Po2 and renal oxygen metabolism were determined in the denervated kidneys of anesthetized rabbits under hypoxic, normoxic, and hyperoxic conditions. During artificial ventilation with 21% oxygen (normoxia), RBF increased 32 ± 8% during renal arterial infusion of acetylcholine and reduced 31 ± 5% during ANG II infusion. Neither infusion significantly altered arterial pressure, tissue Po2 in the renal cortex or medulla, nor renal oxygen consumption. However, fractional oxygen extraction fell as RBF increased and the ratio of oxygen consumption to sodium reabsorption increased during ANG II infusion. Ventilation with 10% oxygen (hypoxia) significantly reduced both cortical and medullary Po2 (60–70%), whereas ventilation with 50% and 100% oxygen (hyperoxia) increased cortical and medullary Po2 (by 62–298 and 30–56%, respectively). However, responses to altered RBF under hypoxic and hyperoxic conditions were similar to those under normoxic conditions. Thus renal tissue Po2 was relatively independent of RBF within a physiological range (±30%). This was not due to RBF-dependent changes in renal oxygen consumption. The observation that fractional extraction of oxygen fell with increased RBF, yet renal parenchymal Po2 remained unchanged, supports the hypothesis that preglomerular diffusional shunting of oxygen from arteries to veins increases with increasing RBF, and so contributes to dynamic regulation of intrarenal oxygenation.

Single-nephron function and renal oxygen consumption during rapid volume expansion

1976 ◽  
Vol 231 (4) ◽  
pp. 1166-1172 ◽  
Author(s):  
SW Weinstein ◽  
J Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Ringer Solution ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Renal Oxygen Consumption ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Renal Sodium Reabsorption

Isotonic volume expansion reduces net filtrate reabsorption in the proximal tubule while increasing it in Henle's loop. To determine the role oxidative metabolism plays in these processes, experiments were performed on rats initially hydropenic and then rapidly volume expanded with isotonic Ringer solution. Whole-kidney sodium reabsorption, oxygen consumption, and single-nephron function were measured simultaneously. During volume expansion, net renal sodium reabsorption increased concomitantly with a fall in oxygen consumption and a reduction in proximal tubular absolute filtrate reabsorption. The increase in quantity of nonreabsorbed filtrate delivered into the loop of Henle greatly exceeded the amount excreted in the urine. Thus, filtrate reabsorption by the distal nephron segments increased. These data provide evidence that acute volume expansion reduces oxygen-dependent active solute transport in the proximal tubule. The increase noted in distal nephron sodium reabsorption appears nonoxygen dependent, energized by anaerobic glycolysis or occurring passively.

Oxygen requirement of renal Na-K-ATPase-dependent sodium reabsorption

1977 ◽  
Vol 232 (2) ◽  
pp. F152-F158 ◽  
Author(s):  
Ole M. Sejersted ◽  
Ȗystein Mathisen ◽  
Fredrik Kiil
Keyword(s):  
Oxygen Consumption ◽  
Transport System ◽  
Sodium Transport ◽  
Sodium Reabsorption ◽  
Oxygen Requirement ◽  
Aortic Constriction ◽  
Renal Oxygen Consumption ◽  
Wide Range ◽  
Before And After ◽  
Renal Oxygen

The oxygen requirement of the Na-K-ATPase-dependent sodium transport system was examined in anesthetized dogs infused with 15% mannitol-Ringer solutions at a rate of 35 ml/min. Because of renal vasodilatation and abolished autoregulation, filtered sodium (FNa) could be varied over a wide range by progressive aortic constriction. Sodium reabsorption.(RNa and renal oxygen consumption (RVo2) varied in proportion to FNa (r> 0.9). Ouabain, which inhibits Na-K-ATPases reduced RVo2 by 45 ± 6%. During subsequent aortic constriction, the ratio ΔRNa/ΔFNa averaged 0.45 (glomerulotubular balance) (r> 0.9), whereas RVo2 was not significantly altered. Comparisons of ΔRNa/ΔFNa before and after ouabain administration, indicate that about half of an increase in sodium delivery to the distal nephron is reabsorbed by the Na-K-ATPase-dependent sodium transport system and that ΔRNa/ΔRVo2 (Na/O2 ratio) of this system averages 14.5 ± 1.3. This Na/O2 ratio corresponds to 2.4 sodium ions transported per ATP dephosphorylated as found in other tissues. autoregulation; ATP; dog; glomerular filtration rate; mannitol; ouabain; renal blood flow; renal oxygen consumption Submitted on February 24, 1976

Oxygen requirement of bicarbonate-dependent sodium reabsorption in the dog kidney

1980 ◽  
Vol 238 (3) ◽  
pp. F175-F180 ◽  
Author(s):  
O. Mathisen ◽  
T. Monclair ◽  
F. Kiil
Keyword(s):  
Oxygen Consumption ◽  
Energy Requirement ◽  
High Plasma ◽  
Sodium Reabsorption ◽  
Oxygen Requirement ◽  
Additional Energy ◽  
Renal Oxygen Consumption ◽  
Dog Kidney ◽  
Anesthetized Dogs ◽  
Renal Oxygen

The ratio between changes in sodium reabsorption and renal oxygen consumption (Na/O2) was measured in anesthetized dogs at high plasma bicarbonate concentration (32 +/- 1 mM); ethacrynic acid was infused continuously to prevent variations in transcellular NaCl reabsorption when sodium reabsorption was altered by varying plasma PCO2 and glomerular filtration rate (GFR). At high plasma PCO2 (110 mmHg) sodium reabsorption varied in proportion to GRF between 50 and 125% of control GFR (glomerulotubular balance). By reducing PCO2 to 20 mmHg, sodium reabsorption was reduced by 50-60% at constant GFR. The Na/O2 ratio was not significantly different during the two procedures and averaged 48 +/- 2. The ratio between changes in NaHCO3 reabsorption and oxygen consumption averaged 17 +/- 1, which is not significantly different from the Na/O2 ratio of Na-K-ATPase-dependent sodium transport. We propose that NaHCO3 is admitted to the cell by Na+/H+ exchange and that sodium is actively transported by Na-K-ATPase across the peritubular cell membrane; NaHCO3 provides the osmotic force for paracellular reabsorption of water and NaCl (bicarbonate-dependent reabsorption) without additional energy requirement.

Determinants of renal tissue hypoxia in a rat model of polycystic kidney disease

2014 ◽  
Vol 307 (10) ◽  
pp. R1207-R1215 ◽  
Author(s):  
Connie P. C. Ow ◽  
Amany Abdelkader ◽  
Lucinda M. Hilliard ◽  
Jacqueline K. Phillips ◽  
Roger G. Evans
Keyword(s):  
Oxygen Consumption ◽  
Kidney Disease ◽  
Oxygen Delivery ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Sodium Reabsorption ◽  
Polycystic Kidney ◽  
Lewis Rats ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

Renal tissue oxygen tension (Po2) and its determinants have not been quantified in polycystic kidney disease (PKD). Therefore, we measured kidney tissue Po2 in the Lewis rat model of PKD (LPK) and in Lewis control rats. We also determined the relative contributions of altered renal oxygen delivery and consumption to renal tissue hypoxia in LPK rats. Po2 of the superficial cortex of 11- to 13-wk-old LPK rats, measured by Clark electrode with the rat under anesthesia, was higher within the cysts (32.8 ± 4.0 mmHg) than the superficial cortical parenchyma (18.3 ± 3.5 mmHg). Po2 in the superficial cortical parenchyma of Lewis rats was 2.5-fold greater (46.0 ± 3.1 mmHg) than in LPK rats. At each depth below the cortical surface, tissue Po2 in LPK rats was approximately half that in Lewis rats. Renal blood flow was 60% less in LPK than in Lewis rats, and arterial hemoglobin concentration was 57% less, so renal oxygen delivery was 78% less. Renal venous Po2 was 38% less in LPK than Lewis rats. Sodium reabsorption was 98% less in LPK than Lewis rats, but renal oxygen consumption did not significantly differ between the two groups. Thus, in this model of PKD, kidney tissue is severely hypoxic, at least partly because of deficient renal oxygen delivery. Nevertheless, the observation of similar renal oxygen consumption, despite markedly less sodium reabsorption, in the kidneys of LPK compared with Lewis rats, indicates the presence of inappropriately high oxygen consumption in the polycystic kidney.

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