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.

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.

Acute unilateral renal denervation in rats with extracellular volume expansion

1977 ◽  
Vol 232 (1) ◽  
pp. F26-F32 ◽  
Author(s):  
E. Bello-Reuss ◽  
E. Pastoriza-Munoz ◽  
R. E. Colindres
Keyword(s):  
Volume Expansion ◽  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Before And After ◽  
Extracellular Volume Expansion

Sodium reabsorption along the nephron was studied before and after acute unilateral denervation of the left kidney in anesthetized rats with extracellular volume expansion. Studies were also performed before and after sham denervation. Denervation increased urine volume (V) from the left kidney from 35.2 to 59.2 mul min-1 (P less than 0.001) and urinary sodium excretion (UNaV) from 6.9 to 11.8 mueq min-1 (P less than 0.001). The control right kidney showed a simultaneous 45% decrease in V and UNaV. Inulin clearance (GFR) and renal plasma flow (RPF) remained unchanged after denervation in both kidneys. Left kidney late proximal (F/P)m decreased from 1.50 to 1.24 (P less than 0.01); single-nephron GFR (SNGFR) remained unchanged. (F/P)m ratios were also decreased in early distal (3.87–2.65, P less than 0.005) and late distal (5.48–3.83, P less than 0.02) convolutions. Fractional and absolute Na reabsorption in the distal convolution did not decrease. GFR, RPF, V, UNa, late proximal (F/P)m, and SNGFR were unchanged in shamdenervated rats. The increases in V and UNa V produced by acute renal denervation in the volume-expanded anesthetized animal are thus caused by further depression of proximal tubular salt and water reabsorption.

Mechanisms of angiotensin II natriuresis and antinatriuresis

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Anesthetized Dogs

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of endothelin-3 on water and sodium excretion during extracellular volume expansion

Peptides ◽  
1998 ◽  
Vol 19 (8) ◽  
pp. 1373-1376 ◽  
Author(s):  
Mónica P. Majowicz ◽  
Marı́a de Los Angeles Costa ◽  
Ana M. Balaszczuk ◽  
Norberto A. Vidal ◽  
Karina A. Bombicino ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Extracellular Volume Expansion ◽  
Endothelin 3 ◽  
Water And Sodium Excretion

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.

Localization of the nephron sites responsible for mineralocorticoid escape in rats

1980 ◽  
Vol 239 (2) ◽  
pp. F149-F153 ◽  
Author(s):  
D. E. Kohan ◽  
F. G. Knox
Keyword(s):  
Volume Expansion ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Deoxycorticosterone Acetate ◽  
Collecting Tubule ◽  
Pars Recta ◽  
Distal Tubules ◽  
Cortical Collecting Tubule

Fractional delivery of sodium (FDNA) from the superficial late distal tubule is increased in deoxycorticosterone acetate-(DOCA) treated rats, which may compensate for a presumed mineralocorticoid-stimulated sodium reabsorption in the cortical collecting tubule. In the present study, late proximal (LPT) and early distal tubules (EDT) were micropunctured during volume expansion in control and DOCA-treated rats. Whereas FDNa to the LPT was similar in the two groups, FDNa to the EDT was greater in DOCA-treated than in control rats. Additionally, LPT and deep loop of Henle (LH) were micropunctured in volume-expanded control and DOCA-treated rats. FDNa to the bend of the LH was increased in DOCA-treated rats compared to controls. These findings indicate that in DOCA escape sodium reabsorption is diminished in the pars recta and/or loop of Henle of superficial nephrons and there is increased delivery to the bend of the loop of deep nephrons. We conclude that mineralocorticoid escape is most likely due to increased sodium delivery to the cortical collecting tubule from both deep and superficial nephrons.

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.

Effect of volume expansion on renal glucose transport in normal and uremic dogs

1979 ◽  
Vol 236 (6) ◽  
pp. F567-F574
Author(s):  
S. F. Wen ◽  
R. W. Stoll
Keyword(s):  
Volume Expansion ◽  
Extracellular Volume ◽  
Distal Tubule ◽  
Proximal Convoluted Tubule ◽  
Glucose Reabsorption ◽  
Urinary Glucose ◽  
Before And After ◽  
Intermediate Segment ◽  
Extracellular Volume Expansion ◽  
Remnant Kidney

Proximal and distal tubule micropuncture studies were performed in normal and uremic remnant-kidney dogs to examine the tubule mechanism of glucose reabsorption before and after 10% extracellular volume expansion. In normal dogs volume expansion markedly inhibited glucose reabsorption in the proximal convoluted tubule, but the ensuing increase in further distal glucose delivery was nearly completely reabsorbed in the intermediate segment (between late proximal tubule and distal tubule). In the uremic, remnant-kidney dogs, glomerulotubular balance for glucose was well maintained in the proximal convoluted tubule despite an adaptive increase in nephron filtration rate. Volume expansion markedly increased glucose delivery out of the proximal convoluted tubule and an incomplete glucose reabsorption in the intermediate segment led to glycosuria. When glucose delivery to the intermediate segment was increased to a comparable degree by subthreshold glucose loading in hydropenic normal dogs, glucose reabsorption in this segment was virtually complete, suggesting that in the volume-expanded uremic dogs glucose reabsorptive capacity in the intermediate segment was reduced. Thus, the intermediate segment appears to play a significant role in the fine regulation of urinary glucose excretion.

Role of prostaglandins on the renal effects of angiotensin and interstitial pressure during volume expansion

1993 ◽  
Vol 265 (6) ◽  
pp. R1469-R1474 ◽  
Author(s):  
J. M. Pinilla ◽  
A. Alberola ◽  
J. D. Gonzalez ◽  
T. Quesada ◽  
F. J. Salazar
Keyword(s):  
Volume Expansion ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibitor ◽  
Extracellular Volume Expansion ◽  
The Right

This study was undertaken to determine, in anesthetized dogs, the role of renal prostaglandins (PG) in mediating the natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during extracellular volume expansion (ECVE) with isotonic saline. It was also determined if the intrarenal angiotensin II (ANG II) effects during ECVE are potentiated by the inhibition of PG synthesis. ECVE induced similar elevations of RIHP, natriuresis, and fractional lithium excretion in dogs treated (n = 7) and not treated with a PG synthesis inhibitor (n = 5). In other experimental groups, the effects of the intrarenal maintenance of ANG II levels (n = 6) by infusing captopril and ANG II into the right renal artery were compared with those induced by the simultaneous infusion of captopril, ANG II, and a PG synthesis inhibitor (n = 6). In response to ECVE, renal blood flow and glomerular filtration rate were similar in both kidneys when ANG II levels were maintained constant and were significantly higher in the left kidney when ANG II levels were maintained constant and PG synthesis was inhibited in the right kidney. However, when compared with the left kidney, the ECVE-induced increments of natriuresis and RIHP in the right kidney were reduced by the same magnitude when intrarenal ANG II was maintained constant with (36 and 53%, respectively) and without (40 and 54%, respectively) the simultaneous PG synthesis inhibition. Our results indicate that during ECVE, renal PGs do not play an important role in mediating the RIHP-induced increments in natriuresis and decrements in proximal sodium reabsorption. (ABSTRACT TRUNCATED AT 250 WORDS)

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