Mechanism of natriuresis following intravascular and extracellular volume expansion

1969 ◽  
Vol 47 (2) ◽  
pp. 153-159 ◽  
Author(s):  
H. Sonnenberg ◽  
S. Solomon
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
Fluid Compartment ◽  
Proximal Tubular ◽  
Extracellular Volume Expansion ◽  
A Site

In clearance studies in rats, increases in filtration rate and electrolyte excretion were observed following both intravascular and extracellular fluid volume expansion. The inulin concentration ratio of proximal tubular fluid to plasma was decreased with extracellular expansion. Neither natriuresis nor fractional sodium reabsorption was related to the degree of intravascular expansion. Microperfusion studies demonstrated a decrease in proximal sodium reabsorption only when both intravascular and extravascular volumes were expanded; net sodium transport was not affected by a blood volume increase alone. From the data it is concluded that in the rat an increase in blood volume is followed by a rise of filtration rate and a fall of fractional reabsorption at a site distal to the proximal tubule, resulting in diuresis and natriuresis. If, in addition, the interstitial fluid compartment is expanded, a direct inhibition of the active transport component of proximal Na+ reabsorption occurs.

Influence of Extracellular Volume Expansion on the Composition of Proximal Tubular Fluid in Man

1971 ◽  
Vol 40 (6) ◽  
pp. 479-486 ◽  
Author(s):  
J. P. Fillastre ◽  
R. Ardaillou ◽  
R. Isaac
Keyword(s):  
Sodium Chloride ◽  
Ethacrynic Acid ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Tubular Reabsorption ◽  
Sodium Reabsorption ◽  
Experimental Conditions ◽  
Bicarbonate Reabsorption ◽  
Proximal Tubular ◽  
Extracellular Volume Expansion

1. Distal blockade by simultaneous administration of ethacrynic acid and chlorothiazide was performed in healthy subjects whose extracellular fluid was expanded by iso-osmotic sodium chloride or bicarbonate. The results obtained were compared with those from non-expanded subjects (Ardaillou & Fillastre, 1969). 2. By this technique urine approximates in composition to proximal tubular fluid and may be used to provide information on its composition. As in other mammals, UNa/PNa and Uosm/Posm were close to 1, whatever the experimental conditions. UCl/PCl was always higher and UHCO3/PHCO3 always less than 1. 3. Extracellular fluid expansion with sodium chloride depresses water and sodium reabsorption as shown by the increase of tubular fluid and the diminution of UInul/PInul and TNa/GFR × PNa where TNa and GFR × PNa are respectively the amounts of sodium reabsorbed and filtered per min. It also decreases bicarbonate proximal Tm. The influence on bicarbonate reabsorption is more marked in alkali-loaded than in acid-loaded subjects. 4. Extracellular fluid expansion with iso-osmotic sodium bicarbonate also depresses water, sodium and bicarbonate reabsorption. These results suggest that chloride administration is not necessary to diminish bicarbonate reabsorption and that tubular reabsorption of bicarbonate depends in part on the state of effective extracellular volume.

A Role for Tubuloglomerular Feedback in Chronic Partial Ureteral Obstruction

Physiology ◽  
1993 ◽  
Vol 8 (2) ◽  
pp. 74-79
Author(s):  
P Morsing
Keyword(s):  
Renal Function ◽  
Arachidonic Acid ◽  
Ureteral Obstruction ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Extracellular Volume ◽  
Tubuloglomerular Feedback ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Extracellular Volume Expansion

Animals with partial ureteral obstruction have an inability to increase urinary output and glomerular filtration rate in response to an extracellular volume expansion. The mechanism may be a paradoxical resetting of tubuloglomerular feedback in the obstructed kidney, which impacts the roles of arachidonic acid metabolites and kinins in renal function.

Interactions between angiotensin and nitric oxide in the renal response to volume expansion

1995 ◽  
Vol 269 (3) ◽  
pp. R504-R510 ◽  
Author(s):  
M. T. Llinas ◽  
J. D. Gonzalez ◽  
F. J. Salazar
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibition ◽  
Renal Response ◽  
Group 2 ◽  
Extracellular Volume Expansion

This study examined, in anesthetized dogs, the possible interactions between nitric oxide (NO) and angiotensin II (ANG II) in mediating the renal response to an extracellular volume expansion (ECVE). It was found that the intrarenal maintenance of ANG II levels (group 1) or the intrarenal NO synthesis inhibition (group 2) did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional lithium excretion (FeLi). In the third group, ANG II synthesis was inhibited during NO synthesis blockade. It was found in this group that the NO synthesis inhibition reduced the ECVE-induced increment in sodium excretion (P < 0.05) but did not modify the ECVE-induced increment in FeLi. These results suggest that the increase of proximal sodium reabsorption induced by the No synthesis inhibition is mediated by endogenous ANG II levels. In the fourth group, it was observed that NO synthesis inhibition, during the intrarenal maintenance of ANG II levels, induced a decrease of renal blood flow (P < 0.05) and reduced the natriuretic response to ECVE to a lower level (P < 0.05) than that observed in groups 1 and 2. The results of this group suggest that endogenous NO modulates the vasoconstrictor and antinatriuretic effects of ANG II during an ECVE. In summary, the results of this study suggest that there is an important interaction between NO and ANG II in mediating the renal response to an ECVE.

Homeostatic efficiency of tubuloglomerular feedback in hydropenia, euvolemia, and acute volume expansion

1993 ◽  
Vol 264 (6) ◽  
pp. F930-F936 ◽  
Author(s):  
S. C. Thomson ◽  
R. C. Blantz
Keyword(s):  
Volume Expansion ◽  
Closed Loop ◽  
Polynomial Regression ◽  
Extracellular Volume ◽  
Tubuloglomerular Feedback ◽  
Maximum Value ◽  
Proximal Tubular ◽  
Extracellular Volume Expansion ◽  
Tubular Flow

We assessed the homeostatic efficiency of the tubuloglomerular feedback (TGF) system in Inactin-anesthetized Munich-Wistar rats by use of perturbation analysis in closed-loop micropuncture studies. Nephrons were studied in vivo under conditions of hydropenia (HYD, n = 17), euvolemia (EUV, n = 23), and acute isoncotic extracellular volume expansion (EXP, n = 15). Proximal tubular flow was perturbed in free-flowing nephrons with a microperfusion apparatus. Flow rate (VM) was measured upstream from the perturbation (VH) by a noninvasive optical technique. The dependence of VM on VH was estimated by polynomial regression. By using fractional compensation (C = -dVM/dVH), as an index of homeostatic efficiency, we constructed efficiency profiles (C vs. VH). At VH = 0, C tended toward higher values with decreasing volume status, although the effect did not achieve significance. The maximum value of C did not differ between groups. The efficiency profiles shifted leftward with each increment in volume (P < 0.03, HYD vs. EXP), suggesting that the TGF system adapts to acute increments in volume by shifting the efficiency profile in favor of a vasodilatory role.

Role of Cyclic AMP in the Natriuresis of Extracellular Fluid Volume Expansion in the Dog

1977 ◽  
Vol 53 (6) ◽  
pp. 563-571
Author(s):  
R. M. Friedler ◽  
C. Descoeudres ◽  
K. Kurokawa ◽  
W.-J. Kreusser ◽  
S. G. Massry
Keyword(s):  
Body Weight ◽  
Cyclic Amp ◽  
Renal Vein ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Net Production ◽  
Extracellular Volume Expansion

1. The effect of extracellular volume expansion (ECVE) on renal production of cyclic AMP was evaluated in 19 thyroparathyroidectomized dogs. ECVE was produced by the infusion of Ringer bicarbonate solution at a rate of 2 ml min−1 kg−1 body weight; cyclic AMP was measured in plasma obtained from the aorta and renal vein and in the urine. 2. During the natriuresis of ECVE urinary excretion of cyclic AMP, the clearance of cyclic AMP, net nephrogenous cyclic AMP added both to urine and to the renal vein and hence total nephrogenous cyclic AMP increased significantly. 3. This rise in net production of cyclic AMP and a significant natriuresis by the kidney persisted for 60–90 min after discontinuation of active ECVE and return of renal plasma flow to normal. 4. The results support the notion that an increase in the production of cyclic AMP by the kidney may play a role in the natriuresis of ECVE.

Distal tubular function in superficial rat tubules during volume expansion

1980 ◽  
Vol 239 (3) ◽  
pp. F228-F232 ◽  
Author(s):  
J. Diezi ◽  
M. Nenniger ◽  
G. Giebisch
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Fluid Delivery ◽  
Distal Tubules ◽  
Extracellular Volume Expansion

Free-flow micropuncture experiments were carried out on superficial late proximal and distal tubules during hydropenic conditions and during extracellular volume expansion. Fluid collected from tubules was analyzed for inulin and sodium. During volume expansion, renal perfusion pressure to one kidney was reduced so that the increase in distal sodium and fluid delivery that normally occurs after saline loading was prevented. Although urinary sodium excretion remained significantly elevated in such kidneys, the rate of sodium reabsorption along the distal tubules was not different from that occurring under nondiuretic conditions. It is concluded that those factors that reduce net sodium transport in the proximal tubule during extracellular volume expansion do not act on superficial distal tubules. Additional factors beyond the distal tubule contribute to increased sodium excretion and can be shown to be activated even when delivery of fluid and sodium out of superficial distal tubules is normal.

scholarly journals Increased NHE3 abundance and transport activity in renal proximal tubule of rats with heart failure

2012 ◽  
Vol 302 (1) ◽  
pp. R166-R174 ◽  
Author(s):  
Bruna H. Inoue ◽  
Leonardo dos Santos ◽  
Thaissa D. Pessoa ◽  
Ednei L. Antonio ◽  
Bruna P. M. Pacheco ◽  
...  
Keyword(s):  
Heart Failure ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Left Ventricular ◽  
Male Rats ◽  
Sodium Reabsorption ◽  
Mrna Levels ◽  
Transport Activity ◽  
Extracellular Volume Expansion

Heart failure (HF) is associated with a reduced effective circulating volume that drives sodium and water retention and extracellular volume expansion. We therefore hypothesized that Na+/H+ exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. HF was induced in male rats by left ventricle radiofrequency ablation. Sham-operated rats (sham) were used as controls. At 6 wk after surgery, HF rats exhibited cardiac dysfunction with a dramatic increase in left ventricular end-diastolic pressure. By means of stationary in vivo microperfusion and pH-dependent sodium uptake, we demonstrated that NHE3 transport activity was significantly higher in the proximal tubule of HF compared with sham rats. Increased NHE3 activity was paralleled by increased renal cortical NHE3 expression at both protein and mRNA levels. In addition, the baseline PKA-dependent NHE3 phosphorylation at serine 552 was reduced in renal cortical membranes of rats with HF. Collectively, these results suggest that NHE3 is upregulated in the proximal tubule of HF rats by transcriptional, translational, and posttranslational mechanisms. Enhanced NHE3-mediated sodium reabsorption in the proximal tubule may contribute to extracellular volume expansion and edema, the hallmark feature of HF. Moreover, our study emphasizes the importance of undertaking a cardiorenal approach to contain progression of cardiac disease.

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