Factors influencing renal sodium reabsorption in volume expansion

Author(s):  
Franklyn G. Knox ◽  
John A. Haas
1977 ◽  
Vol 233 (5) ◽  
pp. F416-F420
Author(s):  
T. F. Knight ◽  
E. J. Weinman

In the rat, infusion of a volume of isotonic saline equal to 2% of body weight resulted in an 82% increase in delivery of filtrate out of the proximal tubule but little or, in some animals, no change in the urinary excretion of sodium. By contrast, further degrees of volume expansion resulted in lesser increases in the distal delivery of filtrate, but were associated with a marked increase in the urinary excretion of sodium. Sixty minutes following completion of volume expansion, while the animals were still in positive sosium balance, the urinary excretion of sodium decreased 52% compared to a decrease of only 24% in the distal delivery of filtrate. During the course of progressive volume expansion and during the recovery phase, there was a dissociation between alterations in sodium reabosrption in the proximal convoluted tubule and in the whole kidney. These studies indicate that although the proximal tubule is more sensitive to changes in the extracellular fluid volume, distal nephron sites are ultimately responsible both for the natriuresis of volume expansion and the relative antinatriuresis of the recovery periods.


1976 ◽  
Vol 231 (4) ◽  
pp. 1166-1172 ◽  
Author(s):  
SW Weinstein ◽  
J Szyjewicz

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.


1978 ◽  
Vol 54 (5) ◽  
pp. 567-572 ◽  
Author(s):  
M. D. Lifschitz

1. Studies in anaesthetized animals suggest that the renal nerves have a role in the regulation of sodium excretion. Urinary sodium excretion decreases when the renal nerves are stimulated and increases after renal denervation or ganglionic blockade. In order to define the role of the renal nerves in the regulation of urinary sodium excretion in awake animals, dogs were prepared with one kidney denervated and the other intact and the bladder split so that urine could be collected from each kidney. Denervation was confirmed by kidney noradrenaline analysis (1·72 ± 0·29 vs 0·18 ± 0·12 nmol/g). 2. These dogs were studied awake with one of two protocols on each of two separate days. In protocol VH, volume expansion (5% body weight) was followed by haemorrhage of 2% body weight. Fractional sodium excretion fell from 4·7 ± 0·5 to 1·1 ± 0·2% on the denervated side and from 5·6 ± 0·6 to 1·4 ± 0·3% on the intact side. Inulin and p-aminohippurate clearance fell similarly on both sides. 3. In protocol HV, haemorrhage of 2% body weight was followed by blood replacement and volume expansion of 5% body weight. In this second protocol fractional sodium excretion during haemorrhage was 0·23 ± 0·07 and 0·24 ± 0·09% for denervated and intact kidneys respectively and increased to 2·04 ± 0·32 and 2·78 ± 0·60 after volume expansion. 4. In both protocols the denervated kidney was able to reabsorb sodium as well as the innervated kidney during haemorrhage and was able to increase fractional sodium excretion as well as the denervated kidney during volume expansion. These results suggest that the renal nerves do not have a significant role in the regulation of sodium excretion in conscious animals.


Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1089-1092 ◽  
Author(s):  
B. Grunfeld ◽  
M. Gimenez ◽  
M. Balzaretti ◽  
L. Rabinovich ◽  
M. Romo ◽  
...  

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Wanzhu Tu ◽  
Hai Liu ◽  
George Eckert ◽  
J Howard Pratt

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.


1977 ◽  
Vol 232 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
M. D. Johnson ◽  
R. L. Malvin

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.


1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios

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


2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i369-i369
Author(s):  
Takahiro Hayasaki ◽  
Takuji Ishimoto ◽  
Tomohito Doke ◽  
Miguel Lanaspa ◽  
Richard Johnson ◽  
...  

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