Cardiac edema in dogs: Proximal tubular and renal function

1979 ◽  
Vol 57 (2) ◽  
pp. 185-192 ◽  
Author(s):  
H. Mandin
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Hydraulic Pressure ◽  
Oncotic Pressure ◽  
Peritubular Capillary ◽  
Filtration Fraction ◽  
Cardiac Edema ◽  
Single Nephron ◽  
Proximal Tubular

In recent dog studies, intrapericardial injection of Freund's adjuvant resulted in sodium retention, pulmonary edema, liver congestion, and ascites. Twenty-two experiments were initiated 6–13 days after pericardial injection. Micropuncture and clearance measurements were made during chronic cardiac tamponade (CCT) and 60 min after pericardiocentesis (PC). Following PC, sodium excretion (UNaV) increased from 12.2 to 41.3 μequiv./min. Glomerular filtration rate (GFR) during CCT was unaltered (from 37.3 to 38.7 mL/min) by PC. Single nephron glomerular filtration rate (sngfr) increased 23% (p < 0.005). Proximal fractional reabsorption (FR) decreased 6% after PC. Kidney filtration fraction (FF) increased from 0.35 to 0.38 (p < 0.01). Superficial nephron FF (six dogs) increased from 0.25 to 0.32 (p < 0.02). Peritubular capillary protein concentrations decreased following PC (from 7.41 to 6.89 g/100 mL), a result of decreasing systemic protein concentrations (from 5.51 to 4.69 g/100 mL). Tubule and capillary hydrostatic pressures (another six dogs) increased 6.2 and 3.3 mmHg, respectively, following PC (p < 0.05 and p < 0.005). The results indicate PC causes increased UNaV. GFR did not appear to influence UNaV. Decreased FR in the proximal tubule is secondary to increased sngfr, absolute absorption (C) remaining unaltered. The behaviour of C is in part explained by diminished capillary oncotic pressure and increased capillary hydraulic pressure.

Increased single-nephron protein excretion after renal ablation in nephrotic rats

1988 ◽  
Vol 255 (6) ◽  
pp. F1243-F1248 ◽  
Author(s):  
T. W. Meyer ◽  
H. G. Rennke
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Hydraulic Pressure ◽  
Nephron Number ◽  
Renal Ablation ◽  
Single Nephron ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

The effects of reducing nephron number in rats with established nephrosis were investigated. Rats received an injection of adriamycin and were divided into three groups with similar values for proteinuria after 4 wk. Group 1 rats were then subjected to sham operation. Group 2 rats were subjected to four-fifths renal ablation, and group 3 rats were subjected to four-fifths renal ablation and then maintained on enalapril. Micropuncture and morphological studies were performed 3 wk later. During this 3-wk period, proteinuria increased slightly in each group. Increased proteinuria in groups 2 and 3 reflected a dramatic increase in remnant nephron proteinuria after renal ablation in nephrotic rats. Increased remnant nephron proteinuria in groups 2 and 3 was associated with increased single-nephron glomerular filtration rate (group 1, 30 +/- 2 nl/min; group 2, 54 +/- 3 nl/min; group 3, 41 +/- 4 nl/min) and increased glomerular volume (group 1, 0.93 +/- 0.05 x 10(6) micron 3; group 2, 1.30 +/- 0.09 x 10(6) micron 3; group 3, 1.27 +/- 0.05 x 10(6) micron 3). The increase in single-nephron glomerular filtration rate after renal ablation in both group 2 and 3 rats was attributable to an increase in glomerular plasma flow (group 1, 119 +/- 14 nl/min; group 2, 217 +/- 18 nl/min; group 3, 183 +/- 13 nl/min) without a significant increase in glomerular transcapillary hydraulic pressure (group 1, 45 +/- 1 mmHg; group 2, 48 +/- 3 mmHg; group 3, 44 +/- 2 mmHg). Group 2 exhibited an increase in systemic blood pressure that was prevented by enalapril treatment in group 3. These studies show that an increase in remnant nephron proteinuria accompanies glomerular hypertrophy and hyperfiltration when nephron number is reduced in nephrotic rats. This increase in remnant nephron proteinuria is not attributable to elevation of systemic or glomerular capillary pressure.

Feedback mediation of SNGFR autoregulation in hydropenic and DOCA- and salt-loaded rats

1979 ◽  
Vol 237 (1) ◽  
pp. F63-F74 ◽  
Author(s):  
L. C. Moore ◽  
J. Schnermann ◽  
S. Yarimizu
Keyword(s):  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Single Nephron ◽  
Proximal Tubular

Tubuloglomerular feedback (TGF) mediation of autoregulation was investigated by measuring the response of single nephron glomerular filtration rate (SNGFR) to changes in arterial pressure (AP) following acute or chronic TGF inhibition. In hydropenic rats with intact TGF, distal SNGFR was 25.0 +/- 1.2 (SE) and 23.9 +/- 1.4 nl/min at AP of 111 and 135 mmHg, respectively. In the same 20 nephrons during proximal tubular microinfusion of furosemide, distal SNGFR was 23.6 +/- 1.4 (n = 16) and 29.7 +/- 1.4 nl/min (n = 20) (P less than 0.001, n = 16) at 112 and 133 mmHg. When determined proximally, SNGFR was 25.6 +/- 1.0 and 29.5 +/- 0.9 nl/min (P less than 0.001, n = 31) at 112 and 157 mmHg; kidney GFR increased similarly. These data and the predictions of a GFR model were then used to estimate autoregulatory efficiency. This analysis indicated that partial autoregulation occurred during TGF inhibition. Therefore, TGF is an essential, but probably not the only, mechanism mediating SNGFR autoregulation.

Maturational development of glomerular ultrafiltration in the rat

1979 ◽  
Vol 236 (5) ◽  
pp. F465-F471 ◽  
Author(s):  
I. Ichikawa ◽  
D. A. Maddox ◽  
B. M. Brenner
Keyword(s):  
Glomerular Filtration Rate ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Hydraulic Pressure ◽  
Oncotic Pressure ◽  
Kidney Weight ◽  
Adult Rats ◽  
Immature Rats ◽  
Single Nephron ◽  
Glomerular Ultrafiltration

To ascertain the cause of low glomerular filtration rate in newborn and immature mammals, we measured glomerular pressures and flows directly in immature (30- to 45-day-old) euvolemic Munich-Wistar rats with surface glomeruli. As with total kidney GFR, single nephron (SN)GFR was found to be significantly lower than in adult rats, on average by 40% when corrected for kidney weight. Equality between efferent oncotic pressure and transglomeruler hydraulic pressure difference (deltaP) was usually achieved in immature rats, indicating that the glomerular capillary ultrafiltration coefficient is not a factor limiting SNGFR and GFR in immature rats. Although the average values for deltaP in immature rats were slightly, albeit significantly, lower than in adults, markedly lower values (79 +/- 5 vs. 136 +/- 10 nl/min per g kidney wt) for glomerular plasma flow rate (QA) proved to be the primary factor responsible for the lower SNGFR and GFR values in immature rats. Considerably higher values for afferent and efferent arteriolar resistances contributed to this low QA state in immature rats.

Effect of atriopeptin II on determinants of glomerular filtration rate in the in vitro perfused dog glomerulus

1986 ◽  
Vol 250 (6) ◽  
pp. F1119-F1122 ◽  
Author(s):  
T. A. Fried ◽  
R. N. McCoy ◽  
R. W. Osgood ◽  
J. H. Stein
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Final Concentration ◽  
Synthetic Analogue ◽  
Filtration Fraction ◽  
Single Nephron ◽  
Series Of Experiments

Atrial natriuretic factor (ANF) is a peptide originally found to be present in extracts of mammalian atria that possess marked natriuretic and diuretic qualities. A number of mechanisms have been suggested to explain these properties. Recently, it has been suggested that ANF may enhance glomerular filtration. In this report, we describe a series of experiments designed to investigate if atriopeptin II, a 23-amino acid synthetic analogue of ANF, increases glomerular filtration rate (GFR) and, if so, the mechanism for this increase. We used the isolated perfused glomerulus technique (n = 6), which allows a single isolated glomerular unit to be perfused and the determinants of single-nephron GFR (SNGFR) to be measured. Two periods were performed in each experiment, the control followed by the experimental. The only difference between the two periods was the addition of atriopeptin II to the experimental perfusate at a final concentration of 5 X 10(-7) M. There was indeed a significant increase in the SNGFR (78 +/- 27 to 108 +/- 29 nl/min, P less than 0.01). This increase was associated with a significant increase in the glomerular capillary hydrostatic pressure (PGC) from 31 +/- 3 to 35 +/- 3 mmHg (P less than 0.05). The filtration fraction also increased in each experiment (from 0.16 +/- 0.3 to 0.25 +/- 0.03, P less than 0.005). Neither the afferent flow nor the efferent arteriolar flow changed, although there was a tendency for both to decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Maintenance and recovery stages of postischemic acute renal failure in humans

2002 ◽  
Vol 282 (2) ◽  
pp. F271-F280 ◽  
Author(s):  
Deepa Ramaswamy ◽  
Geraldine Corrigan ◽  
Catherine Polhemus ◽  
Derek Boothroyd ◽  
John Scandling ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Control Group ◽  
Hydraulic Pressure ◽  
Structural Controls ◽  
Single Nephron

Postischemic injury in 38 recipients of 7-day-old cadaveric renal allografts was classified into sustained ( n = 15) or recovering ( n = 23) acute renal failure (ARF) according to the prevailing inulin clearance. Recipients of long-standing allografts that functioned optimally ( n = 16) and living transplant donors undergoing nephrectomy ( n = 10) served as functional and structural controls, respectively. A combination of physiological and morphometric techniques were used to evaluate glomerular filtration rate and its determinants 1–3 h after reperfusion and again on day 7 to elucidate the mechanism for persistent hypofiltration in ARF that is sustained. Glomerular filtration rate in the sustained ARF group on day 7 was depressed by 90% (mean ± SD); the corresponding fall in renal plasma flow was proportionately less. Neither plasma oncotic pressure nor the single-nephron ultrafiltration coefficient differed between the sustained ARF and the control group, however. A model of glomerular ultrafiltration and a sensitivity analysis were used to compute the prevailing transcapillary hydraulic pressure gradient (ΔP), the only remaining determinant of ΔP. This revealed that ΔP varied between 27 and 28 mmHg in sustained ARF and 32–38 mmHg in recovering ARF on day 7 vs. 47–54 mmHg in controls. Sustained ARF was associated with persistent tubular dilatation. We conclude that depression of ΔP, perhaps due partially to elevated tubule pressure, is the predominant cause of hypofiltration in the maintenance stage of ARF that is sustained for 7 days.

scholarly journals Nephron filtration rate and proximal tubular fluid reabsorption in the Akita mouse model of type I diabetes mellitus

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 83 ◽  
Author(s):  
Jurgen Schnermann ◽  
Mona Oppermann ◽  
Yuning Huang
Keyword(s):  
Diabetes Mellitus ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Type I Diabetes ◽  
Type I ◽  
Fluid Reabsorption ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption

An increase of glomerular filtration rate (hyperfiltration) is an early functional change associated with type I or type II diabetes mellitus in patients and animal models. The causes underlying glomerular hyperfiltration are not entirely clear. There is evidence from studies in the streptozotocin model of diabetes in rats that an increase of proximal tubular reabsorption results in the withdrawal of a vasoconstrictor input exerted by the tubuloglomerular feedback (TGF) mechanism. In the present study, we have used micropuncture to assess single nephron function in wild type (WT) mice and in two strains of type I diabetic Ins2+/- mice in either a C57Bl/6 (Akita) or an A1AR-/- background (Akita/A1AR-/-) in which TGF is non-functional. Kidney glomerular filtration rate (GFR) of anesthetized mice was increased by 25% in Akita mice and by 52% in Akita/A1AR-/-, but did not differ between genotypes when corrected for kidney weight. Single nephron GFR (SNGFR) measured by end-proximal fluid collections averaged 11.8 ± 1 nl/min (n=17), 13.05 ± 1.1 nl/min (n=23; p=0.27), and 15.4 ± 0.84 nl/min (n=26; p=0.009 compared to WT; p=0.09 compared to Akita) in WT, Akita, and Akita/A1AR-/- mice respectively. Proximal tubular fluid reabsorption was not different between WT and diabetic mice and correlated with SNGFR in all genotypes. We conclude that glomerular hyperfiltration is a primary event in the Akita model of type I diabetes, perhaps driven by an increased filtering surface area, and that it is ameliorated by TGF to the extent that this regulatory system is functional.

Effect of parathyroid hormone on the determinants of glomerular filtration in dogs

1985 ◽  
Vol 248 (4) ◽  
pp. F482-F486 ◽  
Author(s):  
G. R. Marchand
Keyword(s):  
Glomerular Filtration Rate ◽  
Parathyroid Hormone ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Apparent Discrepancy ◽  
Oncotic Pressure ◽  
Concomitant Increase ◽  
Filtration Pressure ◽  
Effective Filtration Pressure ◽  
Single Nephron

Elevated levels of parathyroid hormone (PTH) often are associated with reduced glomerular filtration rate (GFR) in humans. Although PTH has been reported to reduce the ultrafiltration coefficient (Kf) in rats, GFR declined only if they were plasma expanded. In contrast, PTH does not reduce GFR in dogs, despite filtration pressure disequilibrium. To evaluate this apparent discrepancy, the determinants of GFR were measured in acutely thyroparathyroidectomized dogs. In the absence (n = 8) and presence (n = 10) of synthetic bovine PTH, GFR was 29 +/- 3 and 26 +/- 2 ml/min; Single nephron glomerular filtration rate was 58 +/- 4 and 51 +/- 3 nl/min; glomerular plasma flow was 248 +/- 22 and 250 +/- 24 nl/min; glomerular capillary pressure was 58 +/- 2 and 61 +/- 3 mmHg; Bowman's space pressure was 19 +/- 2 and 19 +/- 1 mmHg; and systemic oncotic pressure was 19 +/- 0.8 and 18 +/- 0.5 mmHg. Average effective filtration pressure (EFP) was significantly greater in the presence (18.6 +/- 1.3 mmHg) than in the absence (14.6 +/- 0.9 mmHg) of PTH. Therefore, Kf per glomerulus calculated from these data was significantly (P less than 0.01) less in the presence than in the absence of PTH (2.91 +/- 0.29 and 3.98 +/- 0.16 nl X min-1 X mmHg-1, respectively). It is concluded that PTH reduced Kf. Whereas this effect predicts reduced GFR in dogs, given filtration pressure disequilibrium, a concomitant increase in EFP maintained GFR in the present study.

Mechanism of angiotensin II-induced proteinuria in the rat

1977 ◽  
Vol 233 (1) ◽  
pp. F13-F21 ◽  
Author(s):  
M. P. Bohrer ◽  
W. M. Deen ◽  
C. R. Robertson ◽  
B. M. Brenner
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Hydraulic Pressure ◽  
Hemodynamic Changes ◽  
Filtration Fraction ◽  
Single Nephron ◽  
Reliable Marker

To investigate the mechanism(s) of angiotensin II-induced proteinuria, polydisperse [3H]dextran (D) (radius = 18-42 A) was infused into seven Munich-Wistar rats before and during intravenous infusion of angiotensin II (AII), 0.35 microgram/kg per min. During AII infusion, UprotV rose approximately twofold, and the fractional clearances of D [(U/P)D/(U/P)In] increased significantly for dextrans with radii greater than 22 A. Single nephron filtration fraction increased, due to a measured rise in the glomerular transcapillary hydraulic pressure difference from 34 to 43 mmHg. Near constancy of single nephron glomerular filtration rate resulted, however, from the offsetting effect of a decrease in glomerular plasma flow rate from 83 to 60 nl/min. These measured hemodynamic changes were found, by the use of pore theory, to account to a large extent for the measured increases in (U/P)D/(U/P)In. In seven other rats, fractional clearances of polyanionic dex-ran sulfate (a more reliable marker of albumin filtration than D) were also found to increase significantly with AII, suggesting that the proteinuria induced by AII can be explained, in large part, by hemodynamic factors.

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