Identification of a Delivery-Related Influence on Proximal Tubular Reabsorption during Expansion with Hyperoncotic Albumin in the Rat

1978 ◽  
Vol 55 (4) ◽  
pp. 369-376
Author(s):  
J. F. Donohoe ◽  
Gertrude S. Lefavour ◽  
S. Cortell ◽  
F. J. Gennari
Keyword(s):  
Fluid Flow ◽  
Flow Rate ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Tubular Reabsorption ◽  
Renal Perfusion Pressure ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Proximal Tubular Reabsorption

1. Proximal tubular fluid flow rate was deliberately reduced to control values in rats after acute volume expansion with hyperoncotic albumin, to determine if the depression of reabsorption by albumin-induced expansion could be uncovered by preventing the associated increase in filtrate delivery. Tubular fluid flow was reduced either by reducing renal perfusion pressures or by diverting fluid from early proximal tubular sites. 2. In the absence of controlled delivery, expansion with hyperoncotic albumin increased nephron filtration rate, reduced the TF/P inulin ratio, but had no effect on absolute reabsorptive rate. When proximal tubular flow rate was returned to control values by a simultaneous early collection, fractional reabsorption remained depressed. By contrast, when tubular flow was maintained at control values by reducing renal perfusion pressure, the large fall in fractional reabsorption was blocked. 3. The results indicate that expansion with hyperoncotic albumin depresses proximal tubular reabsorption independently of delivery rate into the proximal tubule, but that this effect can be reversed by a reduction in renal perfusion pressure. These observations unify the results of previous studies and indicate the presence of a delivery-related influence on proximal reabsorption. The inability to detect a reduction in absolute reabsorption when nephron filtration rate is increased during expansion with hyperoncotic albumin is probably due to the countervailing influence of increased delivery rate, which raised reabsorptive rate.

ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

2004 ◽  
Vol 286 (5) ◽  
pp. R865-R873 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Paul Peter Leyssac ◽  
Max Salomonsson ◽  
Ole Skott ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Over Time

Previous experiments from our laboratory showed that longer-lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma ANG II concentration ([ANG II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anesthetized Sprague-Dawley rats during a 30-min reduction in RPP to 88 mmHg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (Pprox), and proximal tubular flow rate (QLP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl]ED), and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 ± 0.3 to 6.0 ± 0.3 ml/min after 5 min (NS) to 5.2 ± 0.2 ml/min after 30 min ( P < 0.05). This decrease occurred in parallel with a gradual increase in PRC from 38.2 ± 11.0 × 10-5 to 87.1 ± 25.1 × 10-5 Goldblatt units (GU)/ml after 5 min ( P < 0.05) to 158.5 ± 42.9 × 10-5 GU/ml after 30 min ( P < 0.01). GFR, Pprox, and [NaCl]ED all decreased significantly after 5 min and remained low. Estimates of pre- and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP, both pre- and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre- and postglomerular resistance due to rising plasma renin and ANG II concentrations.

Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney

1988 ◽  
Vol 255 (3) ◽  
pp. F391-F396 ◽  
Author(s):  
J. D. Firth ◽  
A. E. Raine ◽  
J. G. Ledingham
Keyword(s):  
Filtration Rate ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Isolated Kidney ◽  
Renal Perfusion Pressure ◽  
Low Concentrations ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

The effect of alteration in renal perfusion pressure on the response of the isolated perfused rat kidney to concentrations of alpha-human atrial natriuretic peptide (ANP) within the pathophysiological range has been examined. At a perfusion pressure of 90 mmHg ANP concentrations of 50, 200, and 1,000 pmol/l were without effect on any parameter tested. At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. At 200 and 1,000 pmol/l larger changes in UNa V and FENa were seen; only at 1,000 pmol/l was a significant effect on GFR observed. In contrast, frusemide (furosemide) at concentrations of 10 and 100 mumol/l was natriuretic at both 90 and 130 mmHg, with lesser absolute but greater proportional changes being seen at the lower pressure. It was concluded 1) the response of the isolated kidney to ANP is critically dependent on perfusion pressure, 2) at elevated levels of perfusion pressure the isolated kidney can respond to levels of ANP within the upper physiological and pathophysiological range.

Flash photolysis of caged nitric oxide inhibits proximal tubular fluid reabsorption in free-flow nephron

2005 ◽  
Vol 289 (2) ◽  
pp. R620-R626 ◽  
Author(s):  
Kay-Pong Yip
Keyword(s):  
Nitric Oxide ◽  
Proximal Tubule ◽  
Flash Photolysis ◽  
Tubular Reabsorption ◽  
Fluid Reabsorption ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Tubular Fluid Reabsorption ◽  
Reabsorption Rate ◽  
Proximal Tubular Reabsorption

A nonobstructing optical method was developed to measure proximal tubular fluid reabsorption in rat nephron at 0.25 Hz. The effects of uncaging luminal nitric oxide (NO) on proximal tubular reabsorption were investigated with this method. Proximal fluid reabsorption rate was calculated as the difference of tubular flow measured simultaneously at two locations (0.8–1.8 mm apart) along a convoluted proximal tubule. Tubular flow was estimated on the basis of the propagating velocity of fluorescent dextran pulses in the lumen. Changes in local tubular flow induced by intratubular perfusion were detected simultaneously along the proximal tubule, indicating that local tubular flow can be monitored in multiple sites along a tubule. The estimated tubular reabsorption rate was 5.52 ± 0.38 nl·min−1·mm−1 ( n = 20). Flash photolysis of luminal caged NO (potassium nitrosylpentachlororuthenate) was induced with a 30-Hz UV nitrogen-pulsed laser. Release of NO from caged NO into the proximal tubule was confirmed by monitoring intracellular NO concentration using a cell-permeant NO-sensitive fluorescent dye (DAF-FM). Emission of DAF-FM was proportional to the number of laser pulses used for uncaging. Photolysis of luminal caged NO induced a dose-dependent inhibition of proximal tubular reabsorption without activating tubuloglomerular feedback, whereas uncaging of intracellular cGMP in the proximal tubule decreased tubular flow. Coupling of this novel method to measure reabsorption with photolysis of caged signaling molecules provides a new paradigm to study tubular reabsorption with ambient tubular flow.

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension

1990 ◽  
Vol 258 (1) ◽  
pp. R77-R81
Author(s):  
R. S. Zimmerman ◽  
R. W. Barbee ◽  
A. Martinez ◽  
A. A. MacPhee ◽  
N. C. Trippodo
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Circulating Levels

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

Impaired preservation of GFR during hypotension in preexistent renal hypoperfusion

1989 ◽  
Vol 256 (2) ◽  
pp. F314-F320
Author(s):  
T. Yoshioka ◽  
A. Yared ◽  
V. Kon ◽  
I. Ichikawa
Keyword(s):  
Capillary Pressure ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Arteriolar Resistance ◽  
Single Nephron

Autoregulation of renal blood flow and filtration rate was studied using micropuncture technique in Munich-Wistar rats with acute water deprivation (AWD) or congestive heart failure (CHF). In the first set of experiments, reduction of renal perfusion pressure to approximately to 70% of its initial value resulted in uncoupling of glomerular plasma flow rate and single-nephron glomerular filtration rate (GFR) (i.e., disproportionally profound fall in the latter) in AWD and CHF rats, whereas both indices changed little in normal control (NC) rats. The profound decrease in single-nephron GFR in AWD and CHF rats was primarily due to a reduction in glomerular capillary pressure (change from base-line value was -29 +/- 2% in AWD, -27 +/- 1% in CHF, and -8 +/- 2% in NC). This profound fall in glomerular capillary pressure in AWD and CHF rats was associated with a reduction in efferent arteriolar resistance, which contrastingly increased in NC. To investigate the mechanism underlying this unique efferent arteriolar responsiveness in AWD and CHF, the response of renal arterioles to exogenous angiotensin II was examined in separate groups of AWD, CHF, and NC. There was a markedly attenuated efferent arteriolar vasoconstrictive response in AWD and CHF (the change of efferent arteriolar resistance in both groups was some 5% of that in NC). Thus impairment in the ability to preserve GFR in these two conditions is attributed, at least in part, to altered efferent arteriolar response in the face of reduced renal perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of renal perfusion pressure on renal interstitial hydrostatic pressure in rats

1989 ◽  
Vol 256 (1) ◽  
pp. F165-F170 ◽  
Author(s):  
A. A. Khraibi ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Polyethylene Matrix ◽  
Renal Perfusion Pressure ◽  
Fractional Excretion Of Sodium

The purpose of this study was to investigate the hypothesis that changes in renal perfusion pressure may be transmitted to the renal interstitium and cause alterations in renal interstitial hydrostatic pressure and sodium excretion. A method that utilizes a chronically implanted polyethylene matrix that allows for direct continuous measurement of renal interstitial hydrostatic pressure, and agrees well with subcapsular measurement in rats, was developed. Renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate were 3.0 +/- 0.3 mmHg, 0.35 +/- 0.13%, and 19.44 +/- 3.00 microliter/min, respectively, when renal perfusion pressure was 101 +/- 0.8 mmHg. When renal perfusion pressure was increased to 123 +/- 0.9 mmHg renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate increased significantly to 5.8 +/- 0.6 mmHg, 1.29 +/- 0.29%, and 50.76 +/- 8.83 microliter/min, respectively, in anesthetized male Sprague-Dawley rats. These changes occur despite a well-autoregulated glomerular filtration rate and renal blood flow. In conclusion, increasing renal perfusion pressure caused a significant increase in renal interstitial hydrostatic pressure as measured directly by the implanted polyethylene matrix method and was associated with a significant increase in sodium excretion.

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