scholarly journals The effect of volume expansion on sodium reabsorption in the diluting segment of the dog kidney

1972 ◽  
Vol 1 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Lewis J. Barton ◽  
L.Henry Lackner ◽  
Floyd C. Rector ◽  
Donald W. Seldin
Keyword(s):  
Volume Expansion ◽  
Sodium Reabsorption ◽  
Diluting Segment ◽  
Dog Kidney

Influence of Hydrostatic and Oncotic Pressure on Sodium Reabsorption in the Unilateral Pyelonephritic Dog Kidney

1974 ◽  
Vol 47 (4) ◽  
pp. 367-376
Author(s):  
J. P. Wagnild ◽  
F. D. Gutmann ◽  
R. E. Rieselbach
Keyword(s):  
Sodium Chloride ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
Oncotic Pressure ◽  
Peritubular Capillary ◽  
Physical Force ◽  
Dog Kidney ◽  
Capillary Fluid ◽  
Diseased Kidney

1. The diseased kidney in the dog with experimental unilateral reduction in nephron population, has been shown previously to undergo an exaggerated inhibition of sodium reabsorption after extracellular fluid (ECF) volume expansion induced by isotonic sodium chloride solution compared with the control kidney. The latter serves to maintain a non-azotaemic environment. 2. In the present studies, manoeuvres designed to alter predominantly either post-glomerular hydrostatic pressure (PGHP) or peritubular capillary oncotic pressure (COP) were performed to investigate further the mechanism of this exaggerated natriuresis. 3. Volume expansion with 5 g/dl albumin in 145 mmol/l sodium chloride (saline), thereby increasing PGHP without changing COP, produced exaggerated diseased kidney natriuresis, but of a smaller magnitude than when the same dogs were studied under a lesser degree of intravascular volume expansion with 145 mmol/l saline. Renal vasodilatation produced by systemically administered dopamine, which increases PGHP without ECF volume expansion, also produced exaggerated natriuresis by the diseased kidney. 4. A selective decrease in COP induced by expansion with saline in conjunction with trimethophan camsylate (Arfonad)-induced hypotension also produced exaggerated diseased kidney natriuresis, but to a lesser degree than saline expansion alone in the same dogs. 5. Thus experimental manoeuvres designed to reduce peritubular capillary fluid reabsorption by either predominantly increasing PGHP or decreasing COP produced exaggerated diseased kidney natriuresis. This exaggerated natriuretic response to manoeuvres which predominantly altered either physical force by itself did not approach the response elicited by expansion with saline. 6. The data suggest that alterations in Starling forces play an important role in mediating the exaggerated diseased kidney natriuresis after an acute saline load.

Exaggerated Phosphaturic Response to Volume Expansion in Patients with Essential Hypertension

1975 ◽  
Vol 49 (3) ◽  
pp. 207-211 ◽  
Author(s):  
C. Chaimovitz ◽  
A. Spierer ◽  
H. Leibowitz ◽  
S. Tuma ◽  
O. S. Better
Keyword(s):  
Volume Expansion ◽  
Chloride Solution ◽  
Sodium Reabsorption ◽  
Water Diuresis ◽  
Diluting Segment ◽  
Hypertensive Patients ◽  
Reabsorptive Capacity ◽  
Proximal Tubular ◽  
Isotonic Sodium Chloride ◽  
Distal Delivery

1. Tubular handling of sodium in hypertensive patients has been evaluated with urinary phosphate excretion used as a marker for proximal tubular reabsorptive capacity. 2. Nine hypertensive patients and nine normal control subjects were studied during sustained water diuresis and the intravenous infusion of isotonic sodium chloride solution to produce volume expansion. 3. In the hypertensive patients there was exaggerated phosphaturia, natriuresis and enhanced distal delivery of sodium. Sodium reabsorption in the diluting segment was normal. 4. The enhanced distal delivery and augmented phosphaturia suggest that a decreased reabsorption of sodium in the proximal tubule is the most likely explanation for the exaggerated natriuretic response to volume expansion in hypertensive patients.

Abstract 360: Increased Aldosterone Sensitivity in Young Blacks

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Wanzhu Tu ◽  
Hai Liu ◽  
George Eckert ◽  
J Howard Pratt
Keyword(s):  
Volume Expansion ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Lower Plasma ◽  
Blacks And Whites ◽  
Small Increments ◽  
Using Data ◽  
Different Levels

Aldosterone contributes to the elevation of blood pressure (BP) by acting on the distal tubule to cause greater sodium retention and volume expansion. Blacks, in comparison with whites, have lower plasma aldosterone concentrations (PAC), possibly due to increased sodium reabsorption and resultant renin suppression, as evidenced by their lower plasma renin activity (PRA); but BP is on average higher in blacks. The seemingly different BP-PAC relationships in blacks and whites raise point to the possibility of different aldosterone sensitivity in the two race groups. Using data from a cohort of normotensive youths (n=654 observations contributed by 537 subjects), we used a varying coefficient model to examine the BP effect of PAC at different levels of PRA in blacks and whites. We characterized the effects of PAC as a function of PRA and assessed its effect on age, sex, and height-adjusted BP percentile. The estimated effects are presented graphically (Figure 1 a&b). Blacks had lower PRA and PAC (PRA: 2.8 vs 3.3, p=0.002; PAC: 8.7 vs 14.1, p<0.0001; PAC/PRA: 4.7 vs 5.4, p=0.172), and marginally higher systolic and diastolic BP percentiles (SBP%: 44.5 vs 40.6, p=0.082; DBP%: 57 vs 51, p=0.004). In blacks, the BP effect of PAC was much greater in blacks at lower PRA levels (p=0.004); in whites, PAC effect on BP was not significant (p=0.164) and the effect did not change noticeably with PRA. In conclusion, the finding supports the notion that blacks have higher levels of aldosterone sensitivity, especially for those with lower PRA. A sustained state of volume expansion appears to make blacks vulnerable to the BP effects of even small increments in sodium retention produced by aldosterone.

Mechanism of exaggerated diuresis in spontaneously hypertensive rats

1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios
Keyword(s):  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978

Studies on Mineralocorticoid ‘Escape’ in Cirrhosis

1979 ◽  
Vol 56 (5) ◽  
pp. 401-406 ◽  
Author(s):  
S. P. Wilkinson ◽  
I. K. Smith ◽  
Helen Moodie ◽  
Lucilla Poston ◽  
R. Williams
Keyword(s):  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
The Other ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Similar Extent ◽  
Water Diuresis ◽  
Diluting Segment

1. The mineralocorticoid 9α-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an ‘escape’ from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the ‘effective’ extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. These findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.

Suppressive action of prolactin on renal response to volume expansion

1975 ◽  
Vol 229 (1) ◽  
pp. 81-85 ◽  
Author(s):  
MS Lucci ◽  
HH Bengele ◽  
S Solomon
Keyword(s):  
Volume Expansion ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Physical Factors ◽  
Water Load ◽  
Renal Response ◽  
Water Handling ◽  
Male Wistar Rats ◽  
Diuretic Response ◽  
Ovine Prolactin

The effects of prolactin on rat renal sodium and water handling during volume expansion were studied using clearance techniques. Both control and experimental adult male Wistar rats were prehydrated with an oral water load of volume equal to 2.5% body weight (BW). At least 3 h later, a continuous intravenous infusion of ovine prolactin (NIH-P-S8), 7.1 mug/h per 100 g, was started in the experimental group. After a 1-h steady-state period, the rats were given an intravenous expansion infusion of either hypotonic saline (2.5% BW), isotonic saline (2.5% and 7.5% BW), or blood (2.5% BW). In all control hypotonic and isotonic saline-expanded animals, within 1 h the rats excreted a volume of urine equal to over 50% of the volume of saline infused. The diuretic and natriuretic responses to saline expansion of prolactin-treated rats were significantly smaller than controls. In contrast to the effects of prolactin on the renal response to saline infusions, it did not alter the natriuretic or diuretic response to blood infusion. Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule.

Effects of certain inhibitors on renal excretion of salt and water

1963 ◽  
Vol 205 (1) ◽  
pp. 117-122 ◽  
Author(s):  
James C. Strickler ◽  
Richard H. Kessler
Keyword(s):  
Atp Synthesis ◽  
Cation Transport ◽  
Sodium Reabsorption ◽  
Antimycin A ◽  
Negative Results ◽  
Renal Oxygen Consumption ◽  
Dog Kidney ◽  
Anesthetized Dogs ◽  
Direct Proportionality

The direct proportionality between renal oxygen consumption and sodium reabsorption suggests a linkage between cation transport and the electron transport system (ETS). We have studied the effects of in vitro inhibitors of the ETS on sodium reabsorption in the dog kidney. Compounds known to block O2 consumption or reduce tissue levels of adenosine triphosphate (ATP) were infused in millimolar quantities into a renal artery of anesthetized dogs. We observed a unilateral diuresis following the administration of cyanide, antimycin-A and iodoacetamide; no diuresis was observed following administration of 2,4-dinitrophenol, azide, and phlorizin. These latter agents block the synthesis or facilitate the degradation of ATP. Negative results were also observed with phthiocol (a naphthoquinone), malonate, and Amytal, inhibitors of specific substrates of ETS. We interpret our results as follows. Inhibition of sodium reabsorption by cyanide and antimycin-A supports the hypothesis that renal cation transport is dependent in part upon oxidative metabolism. The failure of phlorizin and 2,4-dinitrophenol to affect sodium reabsorption suggests that cation transport may be independent of ATP synthesis or concentration in renal tissues.

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