scholarly journals Effect of peritubular capillary perfusion rate on proximal sodium reabsorption

1972 ◽  
Vol 1 (6) ◽  
pp. 397-405 ◽  
Author(s):  
Norman Bank ◽  
Hagop S. Aynedjian ◽  
Takao Wada
Keyword(s):  
Sodium Reabsorption ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Perfusion Rate ◽  
Peritubular Capillary Perfusion

Disruption of renal peritubular blood flow in lipopolysaccharide-induced renal failure: role of nitric oxide and caspases

2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Saline Group ◽  
No Production ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Synthase Inhibitor ◽  
Peritubular Capillary Perfusion

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.

Enhanced tubuloglomerular feedback during peritubular infusions of angiotensins I and II

1988 ◽  
Vol 255 (3) ◽  
pp. F383-F390 ◽  
Author(s):  
K. D. Mitchell ◽  
L. G. Navar
Keyword(s):  
De Novo ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Angiotensin I ◽  
Peritubular Capillary ◽  
Perfusion Rate ◽  
Flow Pressure ◽  
Stop Flow ◽  
Feedback Responses

Experiments were performed in pentobarbital sodium-anesthetized rats to determine whether increases in intrarenal generation of angiotensin II (ANG II) can enhance the sensitivity of the tubuloglomerular feedback mechanism. Stop-flow pressure (SFP) feedback responses to step increases in late proximal perfusion rate were obtained during control conditions and during simultaneous peritubular capillary infusion of either angiotensin I (ANG I) or ANG II. Infusion of either 10(-7) M ANG II or 10(-5) M ANG I, at rates (18.3 +/- 0.9 and 14.8 +/- 1.5 nl/min, respectively) that did not affect resting SFP, enhanced the magnitude of SFP feedback responses both at a low proximal perfusion rate of 10 nl/min (2.9 +/- 0.9 vs. 0.3 +/- 0.2 and 4.5 +/- 1.0 vs. 0.1 +/- 0.1 mmHg, respectively) and at proximal perfusion rates (greater than 30 nl/min) that elicited a maximal feedback response (13.1 +/- 1.0 vs. 10.1 +/- 0.7 and 13.5 +/- 1.6 vs. 9.8 +/- 0.8 mmHg, respectively). With a higher ANG I infusion rate (20 nl/min), control SFP measured in the absence of distal volume delivery decreased from 39.2 +/- 0.6 to 12.0 +/- 2.8 mmHg (n = 18). These effects were blocked when the ANG II receptor antagonist, saralasin (10(-5) M, Sar), was added to the infusate. In addition, the magnitude of the maximal SFP feedback response was not altered during infusion of Sar alone or ANG I + Sar. These findings indicate that ANG II, either added or formed de novo beyond the glomerular circulation, can enhance the sensitivity of the tubuloglomerular feedback mechanism.

Influence of Hydrostatic and Oncotic Pressure on Sodium Reabsorption in the Unilateral Pyelonephritic Dog Kidney

1974 ◽  
Vol 47 (4) ◽  
pp. 367-376
Author(s):  
J. P. Wagnild ◽  
F. D. Gutmann ◽  
R. E. Rieselbach
Keyword(s):  
Sodium Chloride ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
Oncotic Pressure ◽  
Peritubular Capillary ◽  
Physical Force ◽  
Dog Kidney ◽  
Capillary Fluid ◽  
Diseased Kidney

1. The diseased kidney in the dog with experimental unilateral reduction in nephron population, has been shown previously to undergo an exaggerated inhibition of sodium reabsorption after extracellular fluid (ECF) volume expansion induced by isotonic sodium chloride solution compared with the control kidney. The latter serves to maintain a non-azotaemic environment. 2. In the present studies, manoeuvres designed to alter predominantly either post-glomerular hydrostatic pressure (PGHP) or peritubular capillary oncotic pressure (COP) were performed to investigate further the mechanism of this exaggerated natriuresis. 3. Volume expansion with 5 g/dl albumin in 145 mmol/l sodium chloride (saline), thereby increasing PGHP without changing COP, produced exaggerated diseased kidney natriuresis, but of a smaller magnitude than when the same dogs were studied under a lesser degree of intravascular volume expansion with 145 mmol/l saline. Renal vasodilatation produced by systemically administered dopamine, which increases PGHP without ECF volume expansion, also produced exaggerated natriuresis by the diseased kidney. 4. A selective decrease in COP induced by expansion with saline in conjunction with trimethophan camsylate (Arfonad)-induced hypotension also produced exaggerated diseased kidney natriuresis, but to a lesser degree than saline expansion alone in the same dogs. 5. Thus experimental manoeuvres designed to reduce peritubular capillary fluid reabsorption by either predominantly increasing PGHP or decreasing COP produced exaggerated diseased kidney natriuresis. This exaggerated natriuretic response to manoeuvres which predominantly altered either physical force by itself did not approach the response elicited by expansion with saline. 6. The data suggest that alterations in Starling forces play an important role in mediating the exaggerated diseased kidney natriuresis after an acute saline load.

Peritubular capillary dysfunction and renal tubular epithelial cell stress following lipopolysaccharide administration in mice

2007 ◽  
Vol 292 (1) ◽  
pp. F261-F268 ◽  
Author(s):  
Liping Wu ◽  
Manish M. Tiwari ◽  
Kurt J. Messer ◽  
Joseph H. Holthoff ◽  
Neriman Gokden ◽  
...  
Keyword(s):  
Renal Failure ◽  
Adhesion Molecule ◽  
Cell Stress ◽  
Intercellular Adhesion Molecule ◽  
Intermittent Flow ◽  
Early Event ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Lps Challenge ◽  
Capillary Dysfunction

The mortality rate for septic patients with acute renal failure is extremely high. Since sepsis is often caused by lipopolysaccharide (LPS), a model of LPS challenge was used to study the development of kidney injury. Intravital video microscopy was utilized to investigate renal peritubular capillary blood flow in anesthetized male C57BL/6 mice at 0, 2, 6, 10, 18, 24, 36, and 48 h after LPS administration (10 mg/kg ip). As early as 2 h, capillary perfusion was dramatically compromised. Vessels with continuous flow were decreased from 89 ± 4% in saline controls to 57 ± 5% in LPS-treated mice ( P < 0.01), and vessels with intermittent flow were increased from 6 ± 2% to 31 ± 5% ( P < 0.01). At 2 h, mRNA for intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 were elevated 50- and 27-fold, respectively, suggesting that vascular inflammation is an early event that may contribute to capillary dysfunction. By 10 h, vessels with no flow increased from 5 ± 2% in saline controls to 19 ± 3% in LPS-treated mice ( P < 0.05). By 48 h, capillary function was returning toward control levels. The decline in functional capillaries preceded the development of renal failure and was paralleled by induction of inducible nitric oxide synthase in the kidney. Using NAD(P)H autofluorescence as an indicator of cellular redox stress, we found that tubular cell stress was highly correlated with the percentage of dysfunctional capillaries ( r 2 = 0.8951, P < 0.0001). These data show that peritubular capillary dysfunction is an early event that contributes to tubular stress and renal injury.

Control mechanisms of bicarbonate transport across the rat proximal convoluted tubule

1982 ◽  
Vol 242 (5) ◽  
pp. F532-F543 ◽  
Author(s):  
Y. L. Chan ◽  
B. Biagi ◽  
G. Giebisch
Keyword(s):  
Glass Electrode ◽  
Disulfonic Acid ◽  
Bicarbonate Transport ◽  
Control Mechanisms ◽  
Capillary Perfusion ◽  
Perfusion Rate ◽  
Luminal Perfusion ◽  
Luminal Flow ◽  
Acute Changes ◽  
Convoluted Tubules

Bicarbonate transport (JHCO3) was studied in rat proximal convoluted tubules by luminal and peritubular microperfusion, and the effects on tubular bicarbonate transport of selective changes in luminal and peritubular bicarbonate concentrations and of changes in luminal flow rate were evaluated. A pH glass electrode was used to measure [HCO3(-)] and gave results similar to those of a microcalorimetric method. Increasing the tubular and peritubular [HCO3(-)] at constant luminal perfusion rate (10 nl.min-1) augmented JHCO3, but JHCO3 increased more when pH changes were prevented by PCO2 adjustments (constant peritubular pH) than when pH was allowed to rise with the increase in [HCO3(-)] (constant PCO2). Elevation of the tubular HCO3(-) load by raising [HCO3(-)] stimulated JHCO3 more than when the HCO3(-) load was raised by enhancing luminal perfusion rate at constant [HCO3(-)] An increase in PCO2 at constant peritubular pH increased JHCO3. Diamox and benzolamide inhibited JHCO3 at luminal concentrations of 2-4 X 10(-4) M, yet a small but significant fraction of JHCO3 remained intact. Capillary perfusion with 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (5 X 10(-4) M) depressed JHCO3 by 70%. Acute changes in luminal and peritubular potassium concentrations (range, 2-6 meq/liter) had no effect on JHCO3, but JHCO3 increased moderately but significantly in severe dietary hypokalemia.

Heterogeneity of intracortical peritubular plasma flow in the rat kidney

1977 ◽  
Vol 233 (4) ◽  
pp. F333-F341 ◽  
Author(s):  
J. B. Coelho
Keyword(s):  
Plasma Flow ◽  
Rat Kidney ◽  
Renal Plasma Flow ◽  
The Other ◽  
Intravenous Bolus ◽  
Peritubular Capillary ◽  
Perfusion Rate ◽  
Group I ◽  
Outer Stripe ◽  
Pah Clearance

The 86 Rb-accumulation technique was adapted to the study of intracortical peritubule plasma flow patterns in the rat kidney. A rapid intravenous bolus of 86Rb (50 micronCi) was given to anesthetized nondiuretic rats. One kidney pedicle was tied at 6 s, the other at 12 s. In group I (1o rats) [3H]PAH clearance was measured prior to the 86Rb bolus. In group II (six rats) 86Rb and [3H]PAH (100 micronCi) were given together. The kidneys were snap-frozen, then sliced at -6 degrees C. There were no differences in renal plasma flow (RPF) as measured by either tracer in either group, no differences in the intracortical distribution of [3H]PAH and 86Rb, and no changes in the 86Rb distribution between 6 and 12 s. Tissue plasma flow (TPF) as measured by 86Rb in ml/min per g was 3.88 +/- 0.22 (SE) (142% of RPF/g kidney wt) for cortex 1 (outermost), 3.90 +/- 0.21 for cortex 2, 3.26 +/- 0.14 for cortex 3 (P less than 0.025), 2.17 for cortex 4 (P less than 0.001), 1.34 for cortex-medulla junction (P less than 0.001), and 0.88 +/- 0.07 for outer stripe (P less than 0.001). Peritubular capillary plasma flow, derived as TPF minus GRF/g in each slice, fell progressively from cortex 1 to outer stripe. This is thought to represent lower perfusion rate of "medullary rays."

scholarly journals Hemodynamic changes in the kidney in a pediatric rat model of sepsis-induced acute kidney injury

2011 ◽  
Vol 301 (1) ◽  
pp. F209-F217 ◽  
Author(s):  
Kathryn A. Seely ◽  
Joseph H. Holthoff ◽  
Samuel T. Burns ◽  
Zhen Wang ◽  
Keshari M. Thakali ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Capillary Perfusion ◽  
Peritubular Capillary ◽  
Rat Pups ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
Cortical Capillaries ◽  
Pediatric Sepsis

Sepsis is a leading cause of acute kidney injury (AKI) and mortality in children. Understanding the development of pediatric sepsis and its effects on the kidney are critical in uncovering new therapies. The goal of this study was to characterize the development of sepsis-induced AKI in the clinically relevant cecal ligation and puncture (CLP) model of peritonitis in rat pups 17–18 days old. CLP produced severe sepsis demonstrated by time-dependent increase in serum cytokines, NO, markers of multiorgan injury, and renal microcirculatory hypoperfusion. Although blood pressure and heart rate remained unchanged after CLP, renal blood flow (RBF) was decreased 61% by 6 h. Renal microcirculatory analysis showed the number of continuously flowing cortical capillaries decreased significantly from 69 to 48% by 6 h with a 66% decrease in red blood cell velocity and a 57% decline in volumetric flow. The progression of renal microcirculatory hypoperfusion was associated with peritubular capillary leakage and reactive nitrogen species generation. Sham adults had higher mean arterial pressure (118 vs. 69 mmHg), RBF (4.2 vs. 1.1 ml·min−1·g−1), and peritubular capillary velocity (78% continuous flowing capillaries vs. 69%) compared with pups. CLP produced a greater decrease in renal microcirculation in pups, supporting the notion that adult models may not be the most appropriate for studying pediatric sepsis-induced AKI. Lower RBF and reduced peritubular capillary perfusion in the pup suggest the pediatric kidney may be more susceptible to AKI than would be predicted using adults models.

Partition Coefficient Ratios and Tumour Perfusion Studied with 85mKr and 133Xe

1987 ◽  
Vol 26 (06) ◽  
pp. 253-257
Author(s):  
M. Mäntylä ◽  
J. Perkkiö ◽  
J. Heikkonen
Keyword(s):  
Partition Coefficient ◽  
Partition Coefficients ◽  
Regional Blood Flow ◽  
Blood Perfusion ◽  
Compartmental Analysis ◽  
Malignant Tumour ◽  
Mean Value ◽  
Perfusion Rate ◽  
Biological Variables ◽  
The Mean

The relative partition coefficients of krypton and xenon, and the regional blood flow in 27 superficial malignant tumour nodules in 22 patients with diagnosed tumours were measured using the 85mKr- and 133Xe-clearance method. In order to minimize the effect of biological variables on the measurements the radionuclides were injected simultaneously into the tumour. The distribution of the radiotracers was assumed to be in equilibrium at the beginning of the experiment. The blood perfusion was calculated by fitting a two-exponential function to the measuring points. The mean value of the perfusion rate calculated from the xenon results was 13 ± 10 ml/(100 g-min) [range 3 to 38 ml/(100 g-min)] and from the krypton results 19 ± 11 ml/(100 g-min) [range 5 to 45 ml/(100 g-min)]. These values were obtained, if the partition coefficients are equal to one. The equations obtained by using compartmental analysis were used for the calculation of the relative partition coefficient of krypton and xenon. The partition coefficient of krypton was found to be slightly smaller than that of xenon, which may be due to its smaller molecular weight.

Thrombin Stimulated Platelet Accumulation on Protein Coated Glass Capillaries: Role of Adhesive Platelet α-Granule Proteins

1989 ◽  
Vol 62 (03) ◽  
pp. 989-995 ◽  
Author(s):  
Juliette N Mulvihill ◽  
J Andrew Davies ◽  
Florence Toti ◽  
Jean-Marie Freyssinet ◽  
Jean-Pierre Cazenave
Keyword(s):  
Human Platelets ◽  
Capillary Perfusion ◽  
Coated Glass ◽  
Bovine Collagen ◽  
Glass Capillaries ◽  
Human Thrombin ◽  
Platelet Accumulation ◽  
Granule Proteins ◽  
Von Willebrand

SummaryThe generation of trace amounts of thrombin at artificial surfaces in contact with blood is likely to be a contributing factor in thrombosis on biomaterials. Using an in vitro capillary perfusion system, platelet accumulation on glass surfaces, uncoated or precoated with purified bovine collagen or human plasma proteins, was determined in the presence or absence of preadsorbed purified human thrombin. Static adsorption for 15 min at 22° C from solutions of thrombin 100 NIH units (33 μg)/ml gave surface concentrations in the range 0.019-0.101 μg/cm2. Protein coated capillaries, thrombin treated or untreated, were perfused for 2 min at 37° C with suspensions of washed 111In-labeled human platelets in Tyrode's-albumin buffer containing 40% washed red blood cells, under conditions of controlled, non pulsatile laminar flow (50 s−1 or 2,000 s−1). Platelet accumulation was increased in the presence of surface adsorbed thrombin on uncoated and albumin or fibrinogen coated glass but little affected on fibronectin or collagen coated glass. On von Willebrand factor (vWF) coated glass, thrombin enhancement was observed only at high shear forces. In experiments using antibodies against human platelet α-granule proteins, thrombin stimulated platelet deposition in uncoated glass capillaries was inhibited at 2,000 s−1 by anti-vWF and to a lesser extent by anti-fibrinogen but not by antithrombospondin antibodies.

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