Effect of volume expansion with NaCl or NaHCO3 on nephron fluid and Cl transport

1977 ◽  
Vol 233 (2) ◽  
pp. F118-F125
Author(s):  
J. H. Galla ◽  
J. E. Beaumont ◽  
R. G. Luke
Keyword(s):  
Proximal Tubule ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Loop Of Henle ◽  
Fluid Reabsorption ◽  
Micropuncture Technique ◽  
Chloride Excretion ◽  
Anion Composition

To assess the influence of plasma anions on nephron fluid and chloride transport following volume expansion (VE), rats were studied by micropuncture technique during hydropenia and after VE with NaCl (CVE) or NaHCO3 (BVE). VE with either solution produced increments in plasma volume, SNGFR, and fractional sodium excretion (FENa), and decrements in proximal and distal TF/P inulin ratio which were not different. The proximal transepithelial chloride ratio decreased similarly in CVE (from 1.34 to 1.16) and BVE (from 1.32 to 1.17). Following VE, proximal fractional Cl reabsorption decreased similarly in both CVE (-5.9%) and BVE (-7.4%). Early distal fractional Cl reabsorption also was decreased in CVE (-12%) but not in BVE (-1%). Fractional chloride excretion increased in CVE but not in BVE. Therefore, following VE plasma anion composition did not significantly modify either fluid reabsorption in proximal tubule or loop of Henle or urinary Na excretion. The fraction of sodium reabsorbed with chloride in the proximal tubule increased, and Cl conservation, primarily within the loop of Henle, can be maintained despite marked natriuresis.

Sodium and chloride transport along the inner medullary collecting duct: effect of saline expansion

1980 ◽  
Vol 238 (6) ◽  
pp. F504-F508 ◽  
Author(s):  
H. H. Bengele ◽  
C. Lechene ◽  
E. A. Alexander
Keyword(s):  
Sodium Chloride ◽  
Sodium Transport ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Collecting Duct ◽  
Urine Flow ◽  
Fluid Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Chloride Excretion ◽  
Medullary Collecting Duct

The effect of volume expansion on inner medullary collecting duct (IMCD) sodium transport remains controversial. Studies employing micropuncture of the IMCD base and tip were interpreted to demonstrate enhanced sodium and chloride reabsorption. Data obtained by microcatheterization evaluating only sodium transport revealed either no reabsorption or net addition. We have examined both sodium and chloride transport by microcatheterization. Volume expansion was comparable to the micropuncture studies: 0.9% saline equal to 10% body wt and then matched to urine flow. The fraction of filtered fluid, sodium, and chloride was analyzed as a function of IMCD length. In eight hydropenic rats 60% of the fluid, 71% of the sodium, and 48% of the chloride delivered to the IMCD was reabsorbed. In six volume-expanded rats no significant net reabsorption of fluid, sodium, or chloride was found. Accordingly, in contrast to the micropuncture results, we have demonstrated that net sodium chloride and fluid reabsorption are absent during volume expansion. We conclude that during volume expansion, fluid, sodium, and chloride excretion increase, in part, because of a reduction in net reabsorption along the IMCD. The degree of volume expansion does not account for the discrepancy between the two techniques.

Effects of Intraluminal sulfate on electrolyte transfers along the perfused rat nephron

1981 ◽  
Vol 59 (2) ◽  
pp. 122-130 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Proximal Tubule ◽  
Chloride Transport ◽  
Distal Tubule ◽  
Phosphate Transport ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Calcium And Magnesium ◽  
A Site ◽  
Distal Delivery

Superficial nephrons were perfused in vivo to determine the effect of intraluminal sulfate (1–20 mM) on electrolyte reabsorption in the rat with special reference to calcium and magnesium transport. This technique allowed us the opportunity of investigating separate electrolyte transfers without alteration of extrarenal influences. The major amount of perfused sulfate was absorbed in the proximal tubule with little absorption distal to the late proximal collection site. Phosphate transport was not affected by high luminal sulfate concentrations indicating distinct reabsorptive mechanisms for these two anions. Intraluminal sulfate significantly inhibited calcium and magnesium reabsorption in the proximal tubule, loop of Henle, and superficial distal tubule, in distinction to modest effects on sodium transport in these nephron segments. Chloride transport was not altered. The inhibition of divalent cation transfer was not quantitively similar in the different tubule segments. Small amounts of sulfate completely inhibited proximal calcium and magnesium reabsorption with little effect on transport within the loop of Henle. Enhanced distal delivery of sulfate significantly inhibited calcium and magnesium reabsorption in the distal tubule, a site where the sulfate anion is not reabsorbed. These results demonstrate the importance of distal delivery of anionic ligands capable of forming nonreabsorbable complexes. Thus distal calcium and magnesium transport may be greatly modified by proximal control of anion reabsorption.

The control of sodium excretion

1978 ◽  
Vol 235 (3) ◽  
pp. F163-F173 ◽  
Author(s):  
H. E. de Wardener
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Collecting Duct ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Salt Loading ◽  
Large Fluctuations

The kidneys of a normal man filter approximately 24,000 meq sodium/day, reabsorb about 23,900, and yet can make a 1--2 meq change in 24-h urinary sodium excretion. The control of urinary sodium excretion, therefore, depends, first, on ensuring that the bulk of the sodium is reabsorbed, a function which is carried out in the proximal tubule and ascending loop of Henle. Second, it depends on adjusting the reabsorption of the small quantity of sodium which is delivered into the collecting duct so that the amount excreted in the urine is that required to maintain sodium balance. The bulk reabsorptive mechanisms can be considered as buffers to prevent large fluctuations in the amount of sodium delivered to the collecting duct, thus facilitating the fine adjustments of reabsorption which are made at this site. In conditions other than extreme salt loading or deprivation, changes in sodium reabsorption in the proximal tubule and loop of Henle probably have little, if any, effect on urinary sodium excretion. Sodium reabsorption in the proximal tubule and the collecting duct appears to be influenced by unidentified circulating substances.

scholarly journals Effect of volume expansion on the paracellular flux of lanthanum in the proximal tubule.

1998 ◽  
Vol 9 (7) ◽  
pp. 1147-1152 ◽  
Author(s):  
C R Ramsey ◽  
T J Berndt ◽  
F G Knox
Keyword(s):  
Proximal Tubule ◽  
Volume Expansion ◽  
Saline Infusion ◽  
Paracellular Transport ◽  
Minor Role ◽  
Fluid Reabsorption ◽  
A Minor ◽  
Electrophysiologic Studies ◽  
Rat Proximal Tubule

Although studies of volume expansion (VE) in the Necturus suggest a major role for paracellular flux in reabsorption by the proximal tubule, results from morphologic or electrophysiologic studies of the effect of VE on the rat proximal tubule suggest only a minor role for paracellular transport. In the present study, during in vivo microperfusion, lanthanum was used as an extracellular marker to determine bidirectional paracellular flux in the rat proximal tubule before and during 10% VE. Lanthanum itself did not affect proximal tubule reabsorption (delta 0.7 +/- 3.3 nl/min, LaCl3 versus saline infusion, n = 7). When lanthanum was added to the luminal perfusate, paracellular lanthanum efflux from the lumen to the interstitium was 28.9 +/- 6.6 pg/min per mm, n = 7. Subsequent VE significantly decreased the paracellular lumen-to-interstitium efflux to 12.8 +/- 8.3 pg/min per mm concomitant with a 49% decrease in proximal fluid reabsorption (delta -2.6 +/- 0.9 nl/min per mm, P < 0.05). When lanthanum was infused interstitially, by means of a chronically implanted matrix, there was significant paracellular lanthanum influx from the interstitium into the lumen (143.9 +/- 18.6 pg/min per mm, n = 4). Subsequent VE significantly increased this interstitium-to-lumen influx to 212.1 +/- 29.2 pg/min per mm as proximal reabsorption was significantly decreased by 58% (delta -2.8 +/- 0.8 nl/min per mm, P < 0.05). Thus, VE affects bidirectional paracellular flux in a manner that would decrease proximal reabsorption; paracellular efflux from the lumen to the interstitium was decreased, whereas paracellular influx from the interstitium to the lumen was increased.

Iso-Oncotic Volume Expansion in the Nephrotic Syndrome

1993 ◽  
Vol 84 (6) ◽  
pp. 627-632 ◽  
Author(s):  
Ton J. Rabelink ◽  
Joost A. Bijlsma ◽  
Hein A. Koomans
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Plasma Volume Expansion ◽  
Humoral Factors

1. In previous studies we found that albumin infusions caused only a modest natriuresis in the nephrotic syndrome, suggesting that hypovolaemia played no part in the sodium retention of these patients. However, this finding was inconclusive, since the hyperoncocity of the infused albumin probably opposed sodium excretion. 2. In the present study, we examined the effect of sustained (68 h) plasma volume expansion (+18%), by means of iso-oncotic albumin infusions, on renal function, blood pressure, humoral factors and sodium balance. 3. Plasma atrial natriuretic peptide levels increased almost threefold and renin-angiotensin system activity was suppressed. Glomerular filtration rate remained unchanged, whereas estimated renal plasma flow increased, resulting in a further decrease in filtration fraction. 4. The increase in plasma volume expansion was accompanied by a modest increase in sodium excretion, which, however, was less than the amount of sodium daily infused with the albumin solutions and consumed with the diet, so that net sodium was retained. 5. This observation supports the concept that an intrinsic renal defect causes the sodium retention in the nephrotic syndrome, and argues against the therapeutic use of albumin infusions.

Hypocalcemia-associated modulation of renal response to acute volume expansion in rats

1987 ◽  
Vol 253 (4) ◽  
pp. F726-F733
Author(s):  
D. E. Wesson
Keyword(s):  
Body Weight ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Wistar Rats ◽  
Prostaglandin Synthesis ◽  
Free Flow ◽  
Renal Response ◽  
Clearance Studies ◽  
Chloride Excretion ◽  
Filtered Load

The present study used free-flow micropuncture and whole-kidney clearance studies to determine the renal response to normocalcemic vs. hypocalcemic acute volume expansion (AVE) in anesthetized Munich-Wistar rats. Animals received AVE with Ringer bicarbonate to 10% body weight; half of these animals were supplemented with calcium to maintain normocalcemia (VE + Ca2+) and half were allowed to become hypocalcemic (VE). Filtered load of chloride and total CO2 (TCO2) to the superficial proximal tubule and delivered load to the superficial loop segment were not different between groups. Superficial proximal tubule absolute Cl reabsorption was not different, but superficial loop segment absolute Cl reabsorption was less in the VE + Ca2+ animals (2,221+/- 106 vs. 2,651+/- 125 pmol/min, P less than 0.05) and whole-kidney fractional chloride excretion was greater (10.5+/- 1.6 vs. 4.3+/- 0.5%, P less than 0.05). When indomethacin (I) was administered to hypocalcemic (VE + I) and normocalcemic (VE + Ca2+ + I) AVE animals, both groups of animals had tubular and whole-kidney chloride reabsorption similar to VE animals. TCO2 reabsorption was not influenced by Ca2+ or I. The data indicate that normocalcemic vs. hypocalcemic AVE results in reduced superficial loop segment chloride reabsorption and greater whole-kidney fractional chloride excretion in the absence but not in the presence of prostaglandin inhibition. The data are compatible with an effect of hypocalcemia during AVE to limit superficial loop segment and whole-kidney chloride excretion by inhibiting renal prostaglandin synthesis.

Effect of acute potassium infusion on loop segment chloride reabsorption in the rat

1983 ◽  
Vol 244 (6) ◽  
pp. F599-F605 ◽  
Author(s):  
K. A. Kirchner
Keyword(s):  
Proximal Tubule ◽  
Plasma Volume ◽  
Filtration Rate ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Distal Tubule ◽  
Fluid Flow Rate ◽  
Single Nephron ◽  
Potassium Loading ◽  
Tubule Fluid

To assess the effect of acute potassium loading on proximal tubule and loop chloride handling, chloride transport was examined in superficial cortical nephrons in control rats and after infusion with either 0.3 M KNO3 (KVE) or 0.3 M NaNO3 (NaVE) using micropuncture techniques. Infusion with either salt increased plasma volume, single nephron glomerular filtration rate (SNGFR), and delivery of fluid and chloride out of the proximal tubule. Plasma volume, tubule fluid-to-plasma inulin ratio, proximal transepithelial chloride ratio, and absolute and fractional proximal chloride delivery, however, were not different in the NaVE and KVE groups. Early distal tubule fluid flow rate, SNGFR, and fluid reabsorption were greater than control values following either infusion but these were not different between KVE and NaVE. Early distal tubule chloride concentration and transepithelial chloride gradient were greater and fractional chloride reabsorption was less in KVE than in either control or NaVE groups. Calculated fractional loop segment chloride reabsorption was less in KVE animals. These data suggest that potassium loading reduces fractional chloride reabsorption in the loop segment of rat superficial cortical nephrons.

scholarly journals Segmental chloride transport in the Dahl-S rat kidney during L-arginine administration.

1995 ◽  
Vol 5 (8) ◽  
pp. 1567-1572
Author(s):  
K A Kirchner ◽  
B A Crosby ◽  
A R Patel ◽  
J P Granger
Keyword(s):  
Sodium Chloride ◽  
Perfusion Pressure ◽  
Chloride Transport ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Fluid Reabsorption ◽  
Nephron Segments ◽  
Single Nephron ◽  
Chloride Excretion ◽  
Pressure Natriuresis

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. The nephron segments responsible for improvement in sodium chloride handling during L-arginine administration are unknown. Micropuncture techniques were used to examine fluid and chloride transport along superficial nephron segments in DS rats maintained on an 8% sodium diet and given L-arginine or vehicle ip for 3 wk. Renal perfusion pressure in vehicle-treated DS rats was reduced to that of L-arginine-treated DS rats with an aortic snare. Dahl salt-resistant (DR) rats receiving vehicle were examined for comparison. In agreement with previous studies, urinary sodium chloride excretion was greater (P < 0.05) in L-arginine DS rats than in vehicle DS rats and not different from DR rats at equivalent renal perfusion pressures. Whole-kidney and single-nephron GFR were not different (P = not significant) among groups. Fractional proximal tubule chloride and fluid reabsorption was not different among groups. Fractional loop chloride reabsorption was greater in vehicle-treated DS rats than in DR rats (58.5 +/- 1.5 versus 46.6 +/- 1.7%; P < 0.05), confirming the enhanced chloride reabsorption at this location in DS rats previously reported. Fractional loop chloride reabsorption was identical in vehicle- and L-arginine-treated DS rats (58.4 +/- 1.4 versus 58.9 +/- 3.9%; P = not significant). Fractional loop fluid reabsorption was not different among groups. Fractional distal fluid and chloride reabsorption was not different between DS rat groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Natriuretic Response to Preferential Plasma Volume Expansion in Normal Unanaesthetized Dogs

1971 ◽  
Vol 40 (1) ◽  
pp. 73-79 ◽  
Author(s):  
J. A. Reyburn ◽  
J. P. Gilmore
Keyword(s):  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urine Flow ◽  
Saline Infusion ◽  
Potassium Excretion ◽  
Plasma Volume Expansion ◽  
Volume Increase

1. The natriuretic response of normally hydrated unanaesthetized dogs to preferential plasma volume expansion was studied, comparing the response to infusion of hyperoncotic dextran in isotonic saline with that to infusion of an identical volume of isotonic saline. 2. Significant increases in urine flow, sodium excretion, sodium filtration and potassium excretion were observed with each type of infusion. 3. The changes with each type of infusion were not significantly different however, even though plasma volume increased significantly following dextran saline infusion. 4. The natriuretic response of normal dogs to preferential plasma volume expansion appears to be commensurate with the saline load infused rather than the induced plasma volume increase.

Effects of NaCl on renin and aldosterone responses to potassium depletion

1983 ◽  
Vol 244 (2) ◽  
pp. E164-E169 ◽  
Author(s):  
T. A. Kotchen ◽  
G. P. Guthrie ◽  
J. H. Galla ◽  
R. G. Luke ◽  
W. J. Welch
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Secretion ◽  
Renin Activity ◽  
Potassium Depletion ◽  
Thick Ascending Limb ◽  
Loop Of Henle

We have previously suggested that renin secretion is inversely related to the magnitude of absorptive chloride transport in the thick ascending limb of the loop of Henle. Potassium depletion inhibits chloride transport at this site in the nephron. Consequently, we studied the effects of varying sodium and chloride intakes on the renin and aldosterone responses to potassium depletion. Potassium depletion prevented suppression of plasma renin activity (PRA) by dietary NaCl loading and augmented the PRA response to NaCl deprivation. PRA was stimulated (P less than 0.01) by selective chloride (without sodium) deprivation, and potassium depletion did not augment this response. Potassium depletion did not interfere with suppression of PRA by albumin-induced volume expansion. Plasma aldosterone was suppressed by potassium depletion, and the effect of potassium depletion on aldosterone was augmented by NaCl deprivation. In conclusion, the magnitude of PRA stimulation and aldosterone suppression by potassium depletion is modulated by dietary NaCl intake. The results are consistent with the hypothesis that potassium depletion stimulates renin release by inhibiting chloride transport in the loop of Henle.

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