Effect of saline expansion on peritubule capillary pressures and reabsorption

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.

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Reduced Renal Papillary Plasma Flow in Non-Ascitic Cirrhotic Rats

Clinical Science ◽

10.1042/cs0850139 ◽

1993 ◽

Vol 85 (2) ◽

pp. 139-145 ◽

Cited By ~ 7

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.

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

Clinical Science ◽

10.1042/cs0860405 ◽

1994 ◽

Vol 86 (4) ◽

pp. 405-409 ◽

Cited By ~ 11

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.

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

AJP Renal Physiology ◽

10.1152/ajprenal.1990.259.4.f565 ◽

1990 ◽

Vol 259 (4) ◽

pp. F565-F572 ◽

Cited By ~ 17

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.

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Electrolyte transport in remnant kidney of the dog: effect of furosemide

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.5.1231 ◽

1976 ◽

Vol 230 (5) ◽

pp. 1231-1238 ◽

Cited By ~ 2

Author(s):

SF Wen ◽

NL Wong ◽

RL Evanson ◽

EA Lockhart ◽

JH Dirks

Keyword(s):

Volume Expansion ◽

Extracellular Volume ◽

Stage Ii ◽

Stage Iii ◽

Contralateral Kidney ◽

Before And After ◽

Extracellular Volume Expansion ◽

Potassium Response ◽

Furosemide Administration ◽

Remnant Kidney

Micropuncture studies were performed in 26 dogs with a unilateral remnant kidney to examine its response to modest extracellular volume expansion and furosemide administration in the presence (Stage II) and absence (Stage III) of an intact contralateral kidney. During hydropenia in 15 Stage II dogs, proximal and distal transport of sodium and potassium was comparable to that of normal dogs (Stage I). Following 3% volume expansion, fractional proximal reabsorption was reduced similarly in Stages I and II. Although a slightly greater reduction in fractional loop reabsorption of sodium in Stage II after volume expansion was not significant, it was significantly greater with furosemide administration. In 11 Stage III dogs, proximal fractional reabsorption was depressed during hydropenia, and the loop sodium response to both volume expansion and furosemide administration was exaggerated. In contrast, greater increase in distal potassium secretion was demonstrated mainly in Stage III but not in Stage II remnant kidneys both before and after the diuretic maneuvers. The observations of exaggerated sodium response to furosemide by the remnant kidney in both Stages II and III but greater potassium response only in Stage III suggest that independent factors are responsible for these adaptations when functioning renal mass is reduced.

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Denervated and intact kidney responses to saline load in awake and anesthetized dogs

AJP Renal Physiology ◽

10.1152/ajprenal.1979.237.4.f262 ◽

1979 ◽

Vol 237 (4) ◽

pp. F262-F267 ◽

Cited By ~ 5

Author(s):

J. Sadowski ◽

J. Kurkus ◽

R. Gellert

Keyword(s):

Volume Expansion ◽

Extracellular Volume ◽

Efferent Nerve ◽

Excretory Function ◽

Saline Loading ◽

Before And After ◽

Anesthetized Dogs ◽

Intact Kidney ◽

The Difference ◽

Extracellular Volume Expansion

The function of the innervated and denervated kidney was examined in clearance studies with unilaterally renal-denervated conscious and anesthetized dogs before and after saline loading. Barbiturate anesthesia distinctly depressed hemodynamics and excretory function of both kidneys and increased the difference between the denervated and innervated organ. In conscious moderately hydrated dogs the denervated kidney excreted slightly more sodium and water, while after saline loading higher excretion was observed on the innervated side. The denervated-to-innervated kidney ratios for UNaV, UNaV/100 ml GFR, and urine flow fell significantly from mean control values of 1.27, 1.27, and 1.20, respectively, to 0.80, 0.87, and 0.77 after extracellular volume expansion. Similar alterations of the ratios were observed in anesthetized dogs, but higher excretion of the denervated kidney persisted after saline loading. It is concluded that the greater natriuretic response of the intact kidney to saline infusion was due to inhibition of sodium-retaining action of renal efferent nerve activity by acute extracellular volume expansion.

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

AJP Renal Physiology ◽

10.1152/ajprenal.1979.236.6.f567 ◽

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.

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.6.r1469 ◽

1993 ◽

Vol 265 (6) ◽

pp. R1469-R1474 ◽

Cited By ~ 9

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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Acute unilateral renal denervation in rats with extracellular volume expansion

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.1.f26 ◽

1977 ◽

Vol 232 (1) ◽

pp. F26-F32 ◽

Cited By ~ 7

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.

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