Effect of Phlorhizin on Renal Glucose and Phosphate Transport in the Dog

1979 ◽  
Vol 57 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Sung-Feng Wen
Keyword(s):  
Proximal Tubule ◽  
Sodium Transport ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Reciprocal Relationship ◽  
Sodium Reabsorption ◽  
Group I ◽  
Glucose Reabsorption ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular

1. Clearance and micropuncture studies were performed in 19 thyroparathyroidectomized dogs to examine the inter-relationship between the renal transport of sodium, glucose and phosphate. 2. All experiments were carried out before and after the intravenous administration of phlorhizin [7 mg (15 μmol)/kg] with a sustaining infusion of the same dose/h. Thirteen dogs were studied during hydropenia (group I) and six dogs in the volume-expanded state (group II). 3. In the proximal tubule, phlorhizin significantly reduced sodium reabsorption in hydropenic dogs, but had no effect in volume-expanded dogs. Proximal tubular glucose reabsorption was completely inhibited by phlorhizin in both groups, but no significant change in phosphate reabsorption was observed. 4. Fractional glucose excretion in the urine reached 83–89% after phlorhizin, values significantly less than 100%, suggesting a residual reabsorption of glucose in a more distal segment or in deep nephrons. The changes in fractional excretion of sodium and phosphate were significantly correlated. 5. The effect of phlorhizin on both sodium and glucose reabsorption in the proximal tubule in hydropenic dogs suggests the existence of a co-transport mechanism, whereas the absence of an effect on sodium transport in volume-expanded dogs despite complete inhibition of glucose reabsorption indicates the existence of a sodium-independent component of net proximal tubular glucose transport. 6. Absence of the effect of phlorhizin on proximal tubular phosphate transport in the face of a significant reduction in sodium reabsorption implies that the reciprocal relationship between glucose and phosphate transport could be masked by the changes in sodium transport. Thus the sodium-phosphate transport relationship may prevail over that of glucose-phosphate in the proximal tubule.

Stop flow analysis of renal function in the monkey

1962 ◽  
Vol 202 (6) ◽  
pp. 1105-1108 ◽  
Author(s):  
Arthur J. Vander ◽  
Edward J. Cafruny
Keyword(s):  
Renal Function ◽  
Proximal Tubule ◽  
Flow Analysis ◽  
Macaque Monkey ◽  
Sodium Reabsorption ◽  
Glucose Reabsorption ◽  
Proximal Tubular ◽  
Potassium Secretion ◽  
Stop Flow ◽  
Ureteral Occlusion

Stop flow analysis has been used to study renal function in the macaque monkey. Mannitol diuresis produced excretion of 58–70% of filtered water and 22–34% of filtered sodium. An absence of water and sodium reabsorption from the proximal tubule during ureteral occlusion was observed in three of four experiments, suggesting that this portion of the monkey nephron cannot transport sodium as efficiently as the canine proximal tubule during osmotic diuresis or that it is less permeable to water. Creatinine secretion was observed and localized to the same portion of the proximal tubule which secretes PAH. Inorganic phosphate and glucose reabsorption also occurred in the proximal tubule. Sodium, chloride, and potassium stop flow patterns were identical to those reported for the dog. Chlorothiazide caused an inhibition of distal tubular sodium reabsorption and an enhancement of potassium secretion in the distal nephron. Proximal tubular activity of the drug could not be evaluated.

Proximal tubule response in aldosterone escape

1989 ◽  
Vol 256 (1) ◽  
pp. R86-R90 ◽  
Author(s):  
J. M. Gonzalez-Campoy ◽  
J. Kachelski ◽  
J. C. Burnett ◽  
J. C. Romero ◽  
J. P. Granger ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
Hormonal Changes ◽  
Proximal Tubular ◽  
Temporal Profiles

The response of the proximal tubule to chronic aldosterone administration (15 micrograms.kg-1.day-1) was evaluated in eight conscious female mongrel dogs. Temporal profiles between hemodynamic and hormonal changes and the fractional excretions of sodium and lithium were established. Aldosterone infusion resulted in a significant decrease in urinary sodium excretion from 9.2 +/- 1.3 to 5.8 +/- 0.9 meq/h after 1 day, returning to normal by the 5th day. These changes in urinary sodium excretion were associated with significant elevations of the mean arterial pressure (MAP) from 105 +/- 5 to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF) from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Plasma renin activity (PRA), on the other hand, was depressed by aldosterone, falling below the level of detectability. The fractional excretion of lithium increased significantly by day 2 of aldosterone infusion (from 29 +/- 3 to 44 +/- 6%), reflecting the proximal tubular response to the above changes. We conclude that the proximal tubule responds to increases in MAP and ANF and decreases in PRA during aldosterone infusion by decreasing sodium reabsorption. Subsequent nephron segments must also respond to the volume expansion produced by aldosterone, since the sustained proximal tubule natriuretic response is insufficient to explain all of escape.

Dissociation of proximal tubular glucose and Na+ reabsorption by amphotericin B

1979 ◽  
Vol 236 (4) ◽  
pp. F392-F397
Author(s):  
P. S. Aronson ◽  
J. P. Hayslett ◽  
M. Kashgarian
Keyword(s):  
Proximal Tubule ◽  
Glucose Uptake ◽  
Amphotericin B ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Na Transport ◽  
Glucose Reabsorption ◽  
Tubular Lumen ◽  
Proximal Tubular ◽  
Necturus Proximal Tubule

The effect of amphotericin B on glucose and Na+ transport was studied in the Necturus proximal tubule and in microvillus membrane vesicles isolated from the rabbit renal cortex. In the Necturus experiments, the rate constants for disappearance of radiolabeled glucose (kG) and mannitol (kM) from the tubular lumen were determined by stop-flow microperfusion. Saturability and Na+-dependence of glucose reabsorption was confirmed, since kG was reduced by raising intratubular glucose from 1 to 5 mM or by replacing intratubular Na+ with choline. Neither maneuver affected kM. Intratubular amphotericin B (10 microgram/ml), previously shown to stimulate active Na+ reabsorption in the Necturus proximal tubule, inhibited kG with no effect on kM. In the membrane vesicle preparation, amphotericin inhibited the uphill glucose uptake which results from imposing a NaCl gradient from outside to inside, but had no effect on glucose uptake in either the absence of Na+ or in the presence of Na+ when there was no Na+ gradient. Amphotericin B stimulated the uptake of Na+ by the vesicles. The observed dissociation of glucose and Na+ transport by amphotericin B is consistent with the concept that proximal tubular glucose reabsorption is energized by the luminal membrane Na+ gradient and is not directly linked to active Na+ transport per se.

Quantitative relationship of renal glucose and sodium reabsorption during ECF expansion

1975 ◽  
Vol 229 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Higgins JT ◽  
AE Meinders
Keyword(s):  
Proximal Tubule ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Quantitative Relationship ◽  
Ringer Solution ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Coupled Transport ◽  
Appearance Time ◽  
Glucose Reabsorption

To investigate the quantitative relationship between glucose and sodium reabsorption during extracellular fluid (ECF) expansion and to examine the possible contribution to glucosuria of passive diffusion of glucose from peritubular blood to tubular fluid, renal clearance studies were carried out in dogs. It was found that ECF expansion with isotonic saline or Ringer solution causes a decrease in the maximal rate of glucose reabsorption (TmGlc), which is inversely and linearly related to fractional sodium excretion (FENa) over a range from less than 1% more than 25% FENa (r equals -0.394, P less than 0.001). A continuous relationship between TmGlc and FENa could be demonstrated as the ECF was expanded in individual animals as well as in pooled data. Infusion of albumin solution to preferentially expand the plasma volume and decrease proximal tubular sodium reabsorption produced a 24% fall in TmGlc suggesting that the proximal tubule is the site of interrelated glucose and sodium reabsorption. After pulse injections into the renal artery, [14-C]glucose and insulin had the same appearance time in the urine, thus failing to demonstrate diffusion of glucose from blood into the tubule in saline-loaded dogs as well as in dogs in normal sodium balance. It is suggested that ECF expansion exerts its effect on glucose reabsorption by inhibiting the coupled transport of glucose and sodium across the epithelium of the renal proximal tubule.

scholarly journals Prenatal programming of rat proximal tubule Na+/H+ exchanger by dexamethasone

2007 ◽  
Vol 292 (3) ◽  
pp. R1230-R1235 ◽  
Author(s):  
Amit Dagan ◽  
Jyothsna Gattineni ◽  
Vodi Cook ◽  
Michel Baum
Keyword(s):  
Proximal Tubule ◽  
Membrane Vesicles ◽  
Sodium Reabsorption ◽  
Prenatal Programming ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Old Rats ◽  
Convoluted Tubules

Prenatal administration of dexamethasone causes hypertension in rats when they are studied as adults. Although an increase in tubular sodium reabsorption has been postulated to be a factor programming hypertension, this has never been directly demonstrated. The purpose of this study was to examine whether prenatal programming by dexamethasone affected postnatal proximal tubular transport. Pregnant Sprague-Dawley rats were injected with intraperitoneal dexamethasone (0.2 mg/kg) daily for 4 days between the 15th and 18th days of gestation. Prenatal dexamethasone resulted in an elevation in systolic blood pressure when the rats were studied at 7–8 wk of age compared with vehicle-treated controls: 131 ± 3 vs. 115 ± 3 mmHg ( P < 0.001). The rate of proximal convoluted tubule volume absorption, measured using in vitro microperfusion, was 0.61 + 0.07 nl·mm−1·min−1 in control rats and 0.93+ 0.07 nl·mm−1·min−1 in rats that received prenatal dexamethasone ( P < 0.05). Na+/H+ exchanger activity measured in perfused tubules in vitro using the pH-sensitive dye BCECF showed a similar 50% increase in activity in proximal convoluted tubules from rats treated with prenatal dexamethasone. Although there was no change in abundance of NHE3 mRNA, the predominant luminal proximal tubule Na+/H+ exchanger, there was an increase in NHE3 protein abundance on brush-border membrane vesicles in 7- to 8-wk-old rats receiving prenatal dexamethasone. In conclusion, prenatal administration of dexamethasone in rats increases proximal tubule transport when rats are studied at 7–8 wk old, in part by stimulating Na+/H+ exchanger activity. The increase in proximal tubule transport may be a factor mediating the hypertension by prenatal programming with dexamethasone.

Tubular function

2015 ◽  
Author(s):  
Marijn Speeckaert ◽  
Joris Delanghe
Keyword(s):  
Fractional Excretion ◽  
Tubular Function ◽  
Tubular Dysfunction ◽  
Renal Fanconi Syndrome ◽  
Glomerular Function ◽  
Diminished Capacity ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular ◽  
Pass Through ◽  
Renal Tubular

Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is characterized by hypophosphataemia, and a variety of other abnormalities characteristics of the renal Fanconi syndrome. Distinguishing the location of the lesion in Renal Tubular Acidosis is considered in Chapter 35.

Unimpaired excretion of an acute salt load in conscious hypoproteinaemic dogs

1988 ◽  
Vol 75 (3) ◽  
pp. 271-276 ◽  
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Protein ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Sodium Reabsorption ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium

1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known. 2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet. 3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate. 4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis. 5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels. 6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.

Characterization of the Natriuresis Caused in Normal Man by Immersion in Water

1972 ◽  
Vol 43 (2) ◽  
pp. 275-287 ◽  
Author(s):  
M. Epstein ◽  
D. C. Duncan ◽  
L. M. Fishman
Keyword(s):  
Water Immersion ◽  
Control Period ◽  
Free Water ◽  
Fractional Excretion ◽  
Normal Male ◽  
Free Water Clearance ◽  
Fractional Excretion Of Sodium ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Normal Man

1. The effects of 4–6 h of water immersion on the renal excretion of water and electrolytes were studied in thirteen normal male subjects in balance on a constant diet containing 150 mEq of Na and 100 mEq of K per day. Each subject was studied during a control period, consisting of quiet sitting, and during water immersion to the neck. 2. Immersion resulted in a natriuresis beginning within the first hour, with the rate of sodium excretion eventually exceeding that of the control period by 3–4-fold; potassium excretion also increased. Despite a progressively negative water balance during the immersion studies, urine flow was greater during the first 4 h and free water clearance was greater during the first 2 h of immersion than during the control study. 3. The demonstration of a highly significant increase in fractional excretion of sodium during immersion suggests that the natriuresis of water immersion is not attributable to changes in filtered sodium load. 4. The prompt onset of the natriuresis, the concomitant kaliuresis and the fact that aldosterone secretion under the conditions of study was probably already suppressed make it unlikely that the natriuresis of water immersion is mediated solely by decreases in aldosterone activity. 5. The data suggest that the natriuresis caused by water immersion is the result of decreased fractional reabsorption of sodium proximal to the renal diluting site. The mechanism whereby increased proximal tubular sodium rejection occurs in relation to immersion remains unclear.

Effect of metabolic acidosis on glucose reabsorption in rats with acute hyperglycemia

1990 ◽  
Vol 68 (1) ◽  
pp. 79-83 ◽  
Author(s):  
P. O. Magner ◽  
M. L. Halperin
Keyword(s):  
Proximal Tubule ◽  
Fractional Excretion ◽  
Electrochemical Gradient ◽  
Osmotic Diuresis ◽  
Acute Hyperglycemia ◽  
Luminal Membrane ◽  
Glucose Reabsorption ◽  
Other Substances ◽  
Hyperglycemic Hyperosmolar Nonketotic Coma ◽  
Filtered Load

The rate of reabsorption of glucose in the kidney is a factor to consider with respect to the degree of hyperglycemia in poorly controlled diabetics. The rate of reabsorption of glucose in the proximal tubule is driven by the electrochemical gradient for sodium across the luminal membrane. This gradient in the proximal tubule is also used to reabsorb a number of other substances, quantitatively the most important being bicarbonate. We wished to explore the hypothesis that acidosis, by reducing the filtered load of bicarbonate and therefore the reabsorption of bicarbonate in the proximal tubule, might permit an increased rate of reabsorption of glucose. Hyperglycemia was induced in rats by the infusion of hypertonic glucose. Reabsorption of glucose was measured by clearance methods and factored for glomerular filtration rate (GFR), which has a direct effect on the reabsorption of glucose. The reabsorption of glucose was increased in the kidney when the reabsorption of bicarbonate in the proximal tubule was decreased by either HCl-induced acidosis or the administration of a carbonic anhydrase inhibitor. This effect was independent of a change in GFR and the fractional excretion of Na, factors that may also lead to changes in the reabsorption of glucose by the kidney.Key words: diabetes mellitus, hyperglycemic hyperosmolar nonketotic coma, diabetic ketoacidosis, proximal convoluted tubule, hyperglycemia, glucosuria, osmotic diuresis.

scholarly journals Modeling oxygen consumption in the proximal tubule: effects of NHE and SGLT2 inhibition

2015 ◽  
Vol 308 (12) ◽  
pp. F1343-F1357 ◽  
Author(s):  
Anita T. Layton ◽  
Volker Vallon ◽  
Aurélie Edwards
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Transport Efficiency ◽  
Pathological Conditions ◽  
Sglt2 Inhibition ◽  
Proximal Tubular ◽  
The Individual ◽  
Do So

The objective of this study was to investigate how physiological, pharmacological, and pathological conditions that alter sodium reabsorption (TNa) in the proximal tubule affect oxygen consumption (QO2) and Na+ transport efficiency (TNa/QO2). To do so, we expanded a mathematical model of solute transport in the proximal tubule of the rat kidney. The model represents compliant S1, S2, and S3 segments and accounts for their specific apical and basolateral transporters. Sodium is reabsorbed transcellularly, via apical Na+/H+ exchangers (NHE) and Na+-glucose (SGLT) cotransporters, and paracellularly. Our results suggest that TNa/QO2 is 80% higher in S3 than in S1–S2 segments, due to the greater contribution of the passive paracellular pathway to TNa in the former segment. Inhibition of NHE or Na-K-ATPase reduced TNa and QO2, as well as Na+ transport efficiency. SGLT2 inhibition also reduced proximal tubular TNa but increased QO2; these effects were relatively more pronounced in the S3 vs. the S1–S2 segments. Diabetes increased TNa and QO2 and reduced TNa/QO2, owing mostly to hyperfiltration. Since SGLT2 inhibition lowers diabetic hyperfiltration, the net effect on TNa, QO2, and Na+ transport efficiency in the proximal tubule will largely depend on the individual extent to which glomerular filtration rate is lowered.

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