Segmental chloride reabsorption during volume expansion and recovery

1981 ◽  
Vol 240 (5) ◽  
pp. F395-F399
Author(s):  
A. U. Sheth ◽  
T. F. Knight ◽  
E. Pace ◽  
H. O. Senekjian ◽  
E. J. Weinman

Clearance and micropuncture studies were performed in Sprague-Dawley and Munich-Wistar rats to examine the nephron sites of chloride reabsorption in animals undergoing sustained volume expansion (SVE) (10% of body wt) with isotonic saline and in animals in which the extracellular fluid volume was expanded to 10% of body wt over 60 min, after which the sustaining saline volume was abruptly discontinued (recovery) (R). Net sodium and chloride balances were not significantly different in R compared with SVE. The fractional excretion of chloride, however, was significantly lower (2.62 +/- 0.25 vs. 4.18 +/- 0.62%, P less than 0.05). In the Sprague-Dawley rats, chloride delivery to the early distal tubule average 18% in both groups. Chloride delivery to the late distal tubule was significantly lower in R (4.39 +/- 0.79%) than in SVE (8.55 +/- 0.76%, P less than 0.005). In the Munich-Wistar rats, samples were obtained from the late distal tubule and base and tip of the papilla. Chloride delivery to the base did not differ from that to the late distal tubule in either group, but was significantly lower in R compared with SVE. These results indicate that the so-called “post-volume expansion” antinatriuresis is the result, at least in part, of enhanced reabsorption in the distal tubule.

1974 ◽  
Vol 46 (3) ◽  
pp. 331-345
Author(s):  
M. Martinez-Maldonado ◽  
G. Eknoyan ◽  
W. N. Suki

1. The functional capacity of Henle's loop was examined during hypotonic, isotonic and hypertonic extracellular fluid volume expansion. To eliminate a possible role of antidiuretic hormone (ADH) in the alteration of free water excretion, rats with congenital diabetes insipidus were used. The infusion of hypotonic saline resulted in a progressive rise in free water clearance (CH2O) throughout the range of urine flow (V) attained. Similar results were obtained in rats treated chronically with deoxycorticosterone acetate (DOCA). The infusion of isotonic saline (sodium chloride, 154 mmol/l) produced an initial rise in CH2O until V represented 10% of the filtered load, after which CH2O appeared to reach a plateau. The limitation of CH2O was more marked when hypertonic saline was infused. Medullary and papillary non-urea solute (NUS) concentration rose progressively with the increasing concentration of the saline solution infused. 2. The greater fractional sodium excretion (FENa) after acute isotonic and hypertonic volume expansion is probably the result of inhibition of sodium reabsorption in the collecting duct, although inhibition in the ascending limb cannot be entirely excluded. The depression of CH2O as a function of V seen during acute isotonic or hypertonic volume expansion can be attributed in part to enhanced water back-diffusion from the collecting duct consequent to the increasing medullary and papillary interstitial NUS concentration, even in the absence of ADH. 3. Chronic expansion of extracellular fluid volume by DOCA administration did not modify the response to hypotonic saline infusion.


1986 ◽  
Vol 251 (5) ◽  
pp. R947-R956 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
D. Villarreal ◽  
R. C. Vari

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.


1977 ◽  
Vol 74 (2) ◽  
pp. 193-204
Author(s):  
J. T. BAKER ◽  
S. SOLOMON

A comparison of the renal response to extracellular fluid volume expansion (5% body weight) was made between 25 normal and 25 chronically hypophysectomized rats. The extracellular fluid compartments averaged 25 ± 1% of body weight in both groups during control, fasted conditions. Extracellular fluid volume increased to 33 ± 1% in hypophysectomized and 34 ± 2% in normal rats during expansion, based on body weight. In addition, filtration fraction was similar in both normal and hypophysectomized rats during control (0·29 ± 0·03 and 0·26 ± 0·02 respectively) and infusion of Ringer–Locke solution (0·24 ± 0·05 and 0·27 ± 0·05 respectively). Thus our results cannot be explained by differences in the degree of expansion or failure to increase filtration in proportion to plasma flow. During infusion of isotonic Ringer–Locke solution, fractional water and sodium excretion both averaged 5·1% in normal rats and only 1·3% and 0·82% respectively in hypophysectomized rats. The ratio of single nephron to whole kidney filtration rate failed to increase as much in hypophysectomized compared with normal rats. Significant increases of fractional volume excretion occurred in both groups by the end of the accessible portion of the proximal tubule. However, fractional water reabsorption was depressed significantly more in normal (mean = 37%) than in hypophysectomized rats (mean = 19%). Fractional water reabsorption in distal tubules was similar in both groups during expansion. Arterial pressure was lower in hypophysectomized rats under control conditions, but showed similar changes during expansion compared with normal rats. Passage time decreased significantly in all groups after Ringer–Locke infusion, but remained prolonged in hypophysectomized rats in proximal and distal tubules. It is concluded that chronic hypophysectomy results in a less efficient renal excretion of volume and sodium chloride load. This inefficiency appears to be related in part to (1) failure of the proximal tubule to depress water reabsorption to a level equivalent to normal rats, and (2) failure to re-distribute flow to outer cortical glomeruli following extracellular fluid volume expansion in hypophysectomized rats.


1977 ◽  
Vol 42 (4) ◽  
pp. 624-629 ◽  
Author(s):  
P. D. Snashall ◽  
W. J. Weidner ◽  
N. C. Staub

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.


1988 ◽  
Vol 255 (5) ◽  
pp. F936-F943 ◽  
Author(s):  
R. V. Paul ◽  
T. Ferguson ◽  
L. G. Navar

To evaluate the role of atrial natriuretic factor (ANF) in the renal response to acute blood volume expansion without hemodilution, a reservoir syringe filled with donor rat blood was connected to the femoral artery and vein of anesthetized Sprague-Dawley rats to allow rapid equilibration of the reservoir with the intravascular blood. Volume expansion with blood from the reservoir in two steps (of 1 and 1.5% body wt, separated by 1 h, n = 5 rats) produced a mean peak increase in plasma immunoreactive ANF from 99 +/- 21 to 1,310 +/- 230 pg/ml (P less than 0.001); plasma ANF levels throughout these experiments correlated significantly with simultaneously measured urine flow (r = 0.74, P less than 0.005) and sodium excretion (r = 0.65, P less than 0.005). Another group (n = 7) underwent the same two-step procedure; after the second volume expansion, high-dose atriopeptin III infusion (0.4 microgram.kg-1.min-1 did not further increase fractional excretion of sodium (3.17 +/- 0.27 to 2.50 + 0.39%, P = NS). In another group (n = 9 rats), the same dose of atriopeptin III was started before any blood volume expansion. After the resulting hypotension was corrected by restoration of blood volume, an additional 1.5% body weight blood volume expansion did not further augment sodium excretion. We conclude that the diuresis and natriuresis, which occur in response to volume expansion without hemodilution, rise and fall in parallel with immunoreactive ANF in the plasma, and that ANF and acute blood volume expansion act on the kidney through a similar, saturable mechanism.


1973 ◽  
Vol 3 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Liliana Gradowska ◽  
Sali Caglar ◽  
Ernest Rutherford ◽  
Herschel Harter ◽  
Eduardo Slatopolsky

Sign in / Sign up

Export Citation Format

Share Document