Reduced Renal Papillary Plasma Flow in Non-Ascitic Cirrhotic Rats

1993 ◽  
Vol 85 (2) ◽  
pp. 139-145 ◽  
Author(s):  
Noemí M. Atuchá ◽  
Tomás Quesada ◽  
Joaquín Garcia-Estañ
Keyword(s):  
Hydrostatic Pressure ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Water Retention ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Arterial Blood ◽  
Extracellular Volume Expansion ◽  
The One

1. The purpose of the present investigation was to determine whether an abnormality of the renal papillary circulation is present in a well-established model of cirrhosis without ascites (carbon tetrachloride/phenobarbital). 2. Compared with the control animals, cirrhotic rats showed a reduced diuretic (61.0 ±5.1 versus 18.0 ±2.5%) and natriuretic (67.8 ±8.3 versus 29.6 ±3.6%) response to a volume expansion (3% body weight infusion of 0.9% NaCl). The volume expansion-induced increase in renal interstitial hydrostatic pressure was also blunted in the cirrhotic rats (control 9.3 ±0.9 versus cirrhotic 6.1±1.0 mmHg) and there were no differences in mean arterial blood pressure, renal blood flow or glomerular filtration rate between control and cirrhotic animals. 3. Papillary plasma flow was determined by the 125I-albumin accumulation technique and expressed as mlmin−1100 g−1. In the basal state, papillary plasma flow was significantly lower in cirrhotic rats (59.1 ±4.4, n = 9) than in the control animals (81.8 ±6.9, n = 9). An isotonic saline expansion similar to the one described above significantly increased papillary plasma flow in control rats (108.4±9.1, n = 7) but did not change it in cirrhotic rats (60.2 ±4.9, n = 6). 4. Our results indicate the existence of a selective alteration in the renal papillary circulation in cirrhotic rats, both in the basal state and after a well-established vasodilatory stimulus. The reduced papillary plasma flow of the cirrhotic animals, probably mediated through changes in renal interstitial hydrostatic pressure, may participate in the sodium and water retention that precedes the development of ascites and may be an important mechanism mediating the blunted renal response to extracellular volume expansion.

Effect of saline expansion on peritubule capillary pressures and reabsorption

1981 ◽  
Vol 240 (2) ◽  
pp. F106-F110 ◽  
Author(s):  
C. E. Ott
Keyword(s):  
Hydrostatic Pressure ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Oncotic Pressure ◽  
Capillary Uptake ◽  
Before And After ◽  
Dog Kidney ◽  
Capillary Pressures ◽  
Extracellular Volume Expansion

The effect of extracellular volume expansion on transcapillary Starling forces, capillary uptake, and the reabsorption coefficient in the peritubule microcirculation of the dog kidney was examined. Micropuncture techniques were used to obtain measurement before and after 4% body wt expansion with isotonic saline. Extracellular volume expansion significantly changed all Starling pressures and capillary uptake. Efferent arteriolar oncotic pressure, interstitial oncotic pressure, and capillary uptake decreased (33.1 +/- 3.3 to 22.1 +/- 4.1 mmHg; 5.2 +/- 0.4 to 4.0 +/- 0.3 mmHg; and 44.9 +/- 9.2 to 28.7 +/- 8.6 nl/min, respectively), whereas capillary hydrostatic pressure and interstitial hydrostatic pressure increased (11.3 +/- 1.2 to 13.7 +/- 1.4 and 5.9 +/- 1.0 to 10.4 +/- 1.2 mmHg, respectively). The calculated reabsorption coefficient was 2.40 during hydropenia and 2.36 nl . min-1 . mmHg-1 following volume expansion. The results show that extracellular volume expansion significantly depresses capillary uptake in the dog and suggest that the decreased uptake can be accounted for totally by changes in transcapillary pressures and a constant reabsorption coefficient.

Effects of Nitric Oxide Inhibition on the Renal Papillary Blood Flow Response to Saline-Induced Volume Expansion in the Rat

1994 ◽  
Vol 86 (4) ◽  
pp. 405-409 ◽  
Author(s):  
Noemí M. Atucha ◽  
Ana Ramírez ◽  
Tomás Quesada ◽  
Joaquán García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Renal Medulla ◽  
Synthesis Inhibitor ◽  
Doppler Flowmetry ◽  
Extracellular Volume Expansion

1. Evidence indicates that nitric oxide (NO) exerts a paracrine influence in the renal medulla. Increases in papillary blood flow are thought to be an important determinant of the renal response to extracellular volume expansion. Therefore, in the present study, we have evaluated the role of NO in mediating papillary blood flow (laser-Doppler flowmetry) and excretory responses to volume expansion with isotonic saline (3% body weight, 15 min). 2. Infusion of the NO synthesis inhibitor Nω-nitro-l-arginine methyl ester (10 μg min−1 kg−1), significantly attentuated the renal diuretic and natriuretic responses to volume expansion as well as the renal hydrostatic interstitial pressure increase induced by this manoeuvre. The percentages of the water and sodium excreted in 1 h by the Nω-nitro-l-arginine methyl ester-pretreated animals were 36% and 40% of the load, whereas those of the control animals were 44% and 65%, respectively. 3. In similar experiments performed in the exposed papilla of Munich Wistar rats, the same dose of Nω-nitro-l-arginine methyl ester reduced basal papillary blood flow and blunted the elevation in papillary blood flow induced by volume expansion (6% versus 16% in the control animals). 4. These results indicate that the inhibition of NO synthesis blunts the renal excretory and papillary responses to volume expansion, suggesting that NO modulates these responses through changes in papillary blood flow and renal interstitial hydrostatic pressure.

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.

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.

Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II

1990 ◽  
Vol 259 (4) ◽  
pp. F565-F572 ◽  
Author(s):  
J. Schnermann ◽  
J. P. Briggs
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Tubuloglomerular Feedback ◽  
Plasma Angiotensin ◽  
Single Nephron ◽  
Saline Administration ◽  
Flow Pressure ◽  
Extracellular Volume Expansion

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.

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)

Effect of Ca++ on renal handling of PO4 identical to: evidence for two reabsorptive mechanisms

1975 ◽  
Vol 229 (4) ◽  
pp. 901-906 ◽  
Author(s):  
MM Popovtzer ◽  
JB Robinette ◽  
KM McDonald ◽  
CK Kuruvila
Keyword(s):  
Serum Calcium ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Single Injection ◽  
Extracellular Volume ◽  
Tubular Reabsorption ◽  
Renal Handling ◽  
Parathyroid Extract ◽  
Urinary Cyclic Amp ◽  
Extracellular Volume Expansion

The effect of hypercalcemia on renal handling of phosphorus was studied in parathyroidectomized rats during 1) extracellular volume expansion with normal saline (0.1 mg/100 g per min) and 2) parathyroid extract infusion (1 U/100 g per h). Hypercalcemia (serum calcium 12-15 mg/100 ml) blunted the phosphaturic response to volume expansion, both when serum calcium was raised acutely during volume expansion and when volume expansion was induced in rats with sustained hypercalcemia. These changes were not associated with significant variations in glomerular filtration rate and serum concentration of phosphorus. Hypercalcemia failed to alter the phosphaturic response and the increase in urinary cyclic AMP excretion following both continuous infusion and a single injection of parathyroid extract. These results are consistent with two components of tubular reabsorption of phosphorus. The first is suppressed by extracellular volume expansion and stimulated by hypercalcemia. The second is suppressed by parathyroid hormone and is not affected by hypercalcemia.

The Effect of Acute Extracellular Volume Expansion on Sodium Chloride Reabsorption in the Diluting Segment in Man

1978 ◽  
Vol 54 (3) ◽  
pp. 333-336
Author(s):  
N. Ish-Shalom ◽  
J. Rapoport ◽  
C. Chaimovitz ◽  
O. S. Better
Keyword(s):  
Glomerular Filtration Rate ◽  
Sodium Chloride ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Extracellular Volume ◽  
Free Water ◽  
Water Diuresis ◽  
Water Formation ◽  
Extracellular Volume Expansion ◽  
Distal Delivery

1. The effect of extracellular volume expansion (ECVE) during water diuresis, and of water diuresis alone, on the formation of free water in man was compared. 2. ECVE reduced free water formation at any given rate of distal delivery compared with water diuresis. Thus, ECVE depresses distal sodium chloride reabsorption. 3. This attenuation of free water formation occurred both when urine flow (V/100 ml glomerular filtration rate) and distal chloride delivery [(Cwater + CCl)/100 ml glomerular filtration rate] were used as the terms for distal delivery. 4. We suggest that the distal depression of sodium chloride reabsorption after ECVE is probably due to a direct inhibition of distal sodium chloride transport mechanisms, and not to the flooding of the diluting site by the poorly reabsorbable bicarbonate ion.

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