scholarly journals ω-3 fatty acids attenuate glomerular capillary hydraulic pressure in rats with renal ablation

1995 ◽  
Vol 48 (6) ◽  
pp. 1792-1800 ◽  
Author(s):  
Paul G. Schmitz ◽  
Pascale L. Lane ◽  
Rashid Dalal ◽  
Kun Zhang ◽  
Behred J. Majidi
Keyword(s):  
Fatty Acids ◽  
Hydraulic Pressure ◽  
Glomerular Capillary ◽  
Renal Ablation

scholarly journals Chronic administration of furosemide augments renal weight and glomerular capillary pressure in normal rats

1998 ◽  
Vol 275 (2) ◽  
pp. F230-F234 ◽  
Author(s):  
Pascale H. Lane ◽  
Larry D. Tyler ◽  
Paul G. Schmitz
Keyword(s):  
Renal Injury ◽  
Wistar Rats ◽  
Chronic Administration ◽  
Relative Increase ◽  
Hydraulic Pressure ◽  
Ang Ii ◽  
Filtration Fraction ◽  
Renal Growth ◽  
Glomerular Capillary ◽  
Arteriolar Resistance

Angiotensin II (ANG II) is believed to promote progressive renal injury via augmented glomerular capillary hydraulic pressure (PGC). Acute volume reduction secondary to diuretic administration increases circulating ANG II and augments PGC, yet the hemodynamic effects of sustained diuretic administration are unknown. Therefore, glomerular micropuncture studies were performed in male Munich-Wistar rats after 6–8 wk of treatment with daily furosemide (F, 40 mg/day), furosemide plus the AT1 receptor antagonist, losartan (F + L, 5 mg/day), or no therapy (C, control). Renal weight was increased in F rats (1.23 ± 0.7 g) vs. C (1.00 ± 0.06 g) or F + L (0.97 ± 0.01 g). In addition, PGC was elevated in F animals (52.1 ± 1.5 mmHg) vs. C (43.7 ± 1.5) or F + L-treated rats (41.3 ± 1.7). F-treated rats were also characterized by a relative increase in efferent arteriolar resistance and filtration fraction. The latter was markedly attenuated in F + L-treated animals. Collectively, these findings are consistent with an ANG II-mediated alteration in intrarenal hemodynamics. In contrast to acute volume manipulations, however, chronic furosemide augmented renal growth, whereas losartan administration completely arrested this phenomenon. Further studies are warranted to determine whether the hemodynamic and growth adaptations elicited by chronic F administration induce or accelerate renal injury.

Local intrarenal vasoconstrictor-vasodilator interactions in mild partial ureteral obstruction

1979 ◽  
Vol 236 (2) ◽  
pp. F131-F140 ◽  
Author(s):  
I. Ichikawa ◽  
B. M. Brenner
Keyword(s):  
Angiotensin Ii ◽  
Flow Rate ◽  
Ureteral Obstruction ◽  
Wistar Rats ◽  
Unilateral Ureteral Obstruction ◽  
Hydraulic Pressure ◽  
Mean Values ◽  
Glomerular Capillary ◽  
Single Nephron ◽  
Systemic Factor

Micropuncture studies were performed in Munich-Wistar rats with surgically created chronic partial unilateral ureteral obstruction (UUO). Mean values for superficial single nephron (SN)GFR, total GFR, and initial glomerular plasma flow rate (QA) in obstructed kidneys were essentially identical to values in nonobstructed kidneys. Nevertheless, glomerular capillary hydraulic pressure (PGC) was significantly higher in obstructed than in nonobstructed kidneys. This increase in PGC served to offset the markedly reduced glomerular capillary ultrafiltration coefficient that was also confined to the kidneys ipsilateral to the ureteral obstruction. During infusion of indomethacin or meclofenamate, SNGFR and QA decreased significantly, in association with elevations in arteriolar resistances in obstructed kidneys, whereas such changes were not observed in nonobstructed kidneys. The results suggest that local intrarenal factors, rather than circulating or systemic factor(s), bring about functional adaptations to partial ureteral obstruction. In particular, an indomethacin- and meclofenamate-sensitive vasodilator (presumably prostaglandin) plays a role in antagonizing the effects of a simultaneously acting vasoconstrictor which, although not identified, displayed the functional properties of angiotensin II.

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.

Atrial natriuretic factor inhibits maximal tubuloglomerular feedback response

1987 ◽  
Vol 252 (5) ◽  
pp. F825-F828 ◽  
Author(s):  
C. L. Huang ◽  
M. G. Cogan
Keyword(s):  
Atrial Natriuretic Factor ◽  
Control Period ◽  
Tubuloglomerular Feedback ◽  
Hydraulic Pressure ◽  
Plasma Protein Concentration ◽  
Glomerular Capillary ◽  
Natriuretic Factor ◽  
Single Nephron ◽  
Flow Pressure ◽  
Atrial Natriuretic

The effect of atrial natriuretic factor (ANF) on maximal tubuloglomerular feedback was assessed in 16 Munich-Wistar rats. When the loop of Henle was not perfused, ANF increased single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) from 32 +/- 2 nl/min and 32 +/- 2 mmHg in the control period to 37 +/- 2 nl/min (P less than 0.05) and 40 +/- 2 mmHg (P less than 0.025) after ANF administration, respectively. Because ANF caused SFP to rise but did not significantly alter plasma protein concentration, the estimated glomerular capillary hydraulic pressure increased. Maximal tubuloglomerular feedback response (examined by increasing orthograde microperfusion of the loop from 0 to 50 nl/min) was significantly inhibited by ANF; changes in SNGFR and SFP during the control state, -9 +/- 2 nl/min and -9 +/- 1 mmHg, were reduced to -4 +/- 2 nl/min (P less than 0.05) and -5 +/- 1 mmHg (P less than 0.05), respectively, after ANF administration. In conclusion, the increase in SNGFR caused by ANF is associated with an increase in glomerular capillary hydraulic pressure and with a blunted maximal tubuloglomerular feedback response.

Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation

1981 ◽  
Vol 241 (1) ◽  
pp. F85-F93 ◽  
Author(s):  
T. H. Hostetter ◽  
J. L. Olson ◽  
H. G. Rennke ◽  
M. A. Venkatachalam ◽  
B. M. Brenner
Keyword(s):  
Left Kidney ◽  
Diet Group ◽  
Normal Diet ◽  
Cell Protein ◽  
Hydraulic Pressure ◽  
Group Iii ◽  
Group I ◽  
Renal Ablation ◽  
Single Nephron ◽  
Group Ii

Micropuncture studies were performed in three groups of male Munich-Wistar rats 1 wk after surgery: group I, eight control rats that underwent laparotomy and were fed a normal diet; group II, nine rats that underwent right nephrectomy and segmental infarction of five-sixths of the left kidney and were fed a normal diet; and group III, seven rats that underwent the same renal ablative procedure and were fed a low protein diet. Single nephron glomerular filtration rate (SNGFR) was higher in the remnant kidney of group II rats compared with group I rats due to higher average values for mean glomerular transcapillary hydraulic pressure difference (delta P) and initial glomerular plasma flow rate (QA) in group II. Glomeruli in remnant kidneys of group II showed striking alterations in morphology, including epithelial cell protein reabsorption droplets, foot process fusion, and mesangial expansion. Group III rats demonstrated a mean SNGFR not statistically different from that of group I, but significantly less than that of group II rats. This lack of absolute hyperfiltration in remnant glomeruli of group III rats relative to group I obtained because QA and delta P did not increase above values found in group I. The glomerular structural lesions seen in group II were also largely attenuated in group III. These studies demonstrate that alterations in glomerular hemodynamics associated with renal ablation are accompanied by structural lesions and suggest that sustained single nephron hyperfiltration may have maladaptive consequences by damaging remnant glomeruli.

Single-nephron adaptations to partial renal ablation in the dog

1990 ◽  
Vol 258 (3) ◽  
pp. F495-F503 ◽  
Author(s):  
S. A. Brown ◽  
D. R. Finco ◽  
W. A. Crowell ◽  
D. C. Choat ◽  
L. G. Navar
Keyword(s):  
Mean Value ◽  
Hydraulic Pressure ◽  
Renal Ablation ◽  
Single Nephron ◽  
Group 3 ◽  
Flow Pressure ◽  
The Mean ◽  
Group 2 ◽  
Stop Flow ◽  
Group 1

Micropuncture and histological studies were performed in dogs to characterize single-nephron adaptations to partial renal ablation. Dogs underwent sham surgery (group 1, n = 6), three-fourths nephrectomy (group 2, n = 10), or seven-eighths nephrectomy (group 3, n = 6). Single-nephron glomerular filtration rate (SNGFR) was 71.0 +/- 4.2 nl/min in group 1, 132.5 +/- 9.6 nl/min in group 2, and 161.8 +/- 12.4 nl/min in group 3 (P less than 0.05). There were parallel increases in single-nephron glomerular plasma flow rate (GPF), with a mean value of 235.3 +/- 20.1 nl/min in group 1, 442.4 +/- 34.4 nl/min in group 2, and 569.6 +/- 73.7 nl/min in group 3 (P less than 0.05, group 1 vs. groups 2 and 3). Glomerular capillary pressure, estimated from the sum of proximal tubule stop-flow pressure and arterial oncotic pressure, was 63.2 +/- 1.9 mmHg in group 1, 73.5 +/- 2.0 mmHg in group 2, and 77.9 +/- 2.2 mmHg in group 3 (P less than 0.05, group 1 vs. groups 2 and 3). The mean glomerular transcapillary hydraulic pressure gradient (delta P) in group 2 was not different from group 1 (46.8 +/- 1.3 vs. 43.9 +/- 1.8 mmHg, NS); however, it was significantly increased in group 3 (50.0 +/- 1.4 mmHg; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Endothelin: a potent renal and systemic vasoconstrictor peptide

1989 ◽  
Vol 256 (6) ◽  
pp. F1051-F1058 ◽  
Author(s):  
A. J. King ◽  
B. M. Brenner ◽  
S. Anderson
Keyword(s):  
Renal Plasma Flow ◽  
Dose Range ◽  
Hydraulic Pressure ◽  
Glomerular Injury ◽  
Intravenous Injections ◽  
Glomerular Capillary ◽  
Arteriolar Resistance ◽  
Potent Vasoconstrictor ◽  
Renal Responses ◽  
Dose Dependent

Endothelin is an endothelial cell-derived peptide recently shown to possess potent vasoconstrictor properties. Bolus intravenous injections of endothelin (5-450 pmol) into anesthetized Munich-Wistar rats induced a marked pressor effect, the magnitude and duration of which were dose dependent. Maximal systemic and renal responses occurred within 20 min and persisted for greater than 90 min in the higher dose range. In response to bolus dosages of 25 pmol or greater, renal plasma flow fell proportionately more than glomerular filtration rate, resulting in an increase in filtration fraction. In micropuncture studies of rats given continuous intravenous infusions of endothelin (0.63 pmol/min), the peptide caused a proportionately greater elevation of efferent than afferent arteriolar resistance, with a marked elevation of glomerular capillary hydraulic pressure and a lower glomerular capillary ultrafiltration coefficient. Endothelin was modestly natriuretic when systemic pressure rose and renal function was not severely impaired. This potent renal and systemic vasoconstrictor may play an important role in glomerular injury and in the pathophysiology of a variety of clinical microvasculopathies.

Transport of molecules across renal glomerular capillaries

1976 ◽  
Vol 56 (3) ◽  
pp. 502-534 ◽  
Author(s):  
B. M. Brenner ◽  
C. Baylis ◽  
W. M. Deen
Keyword(s):  
Driving Force ◽  
Molecular Size ◽  
Colloid Osmotic Pressure ◽  
Capillary Network ◽  
Hydraulic Pressure ◽  
Glomerular Injury ◽  
Glomerular Capillary ◽  
Direct Measurements ◽  
Transport Of Macromolecules ◽  
Glomerular Capillaries

Direct measurements of the pressures and flows governing the formation of glomerular ultrafiltrate have been made possible in recent years by virtue of 1) the discovery of rats and monkeys possessing glomerular capillaries on the renal cortical surface, accessible to micropuncture, and 2) technological advances that permit measurement of intracapillary hydraulic pressure and assessment of the change in colloid osmotic pressure along the glomerular capillary network. Based on these direct measurements, evidence has been obtained to indicate that glomerular capillary hydraulic pressure and hence the net driving force for ultrafiltration are lower than previously believed. By the efferent end of the glomerular capillary network, net filtration of fluid ceases, owing to a reduction in the net driving force to zero. Evidence in the rat indicates that the process of ultrafiltration is highly dependent on glomerular plasma flow rate. Studies in rats with surface glomeruli have also made possible an assessment of the factors that govern the transport of macromolecules across the highly specialized capillary network. In addition to molecular size, transcapillary movement of macromolecules is influenced by the glomerular filtration rate, since total transport reflects the combined contributions of convection as well as diffusion. Molecular charge has also been found to be an important determinant of the transport of macromolecules, very likely contributing to the marked restriction to the transcapillary movement of albumin. This electrostatic restriction to the transport of polyanions such as albumin, by some fixed, negatively charged component(s) of the glomerular capillary wall, is markedly reduced in primary glomerular injury. Evidence indicates that glomerular injury results in loss of these fixed negative charges from the capillary walls, providing an attractive explanation for the enhanced filtration of albumin, and hence the proteinuria, observed in a variety of glomerulopathic states.

scholarly journals Pathogenesis of glomerular injury in the fawn-hooded rat: early glomerular capillary hypertension predicts glomerular sclerosis.

1993 ◽  
Vol 3 (11) ◽  
pp. 1775-1782 ◽  
Author(s):  
J L Simons ◽  
A P Provoost ◽  
S Anderson ◽  
J L Troy ◽  
H G Rennke ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Rapid Development ◽  
Systemic Hypertension ◽  
Glomerular Sclerosis ◽  
Hydraulic Pressure ◽  
Glomerular Capillary ◽  
Morphological Studies ◽  
Glomerular Capillary Hypertension ◽  
Segmental Glomerular Sclerosis

Fawn-hooded rats spontaneously develop focal and segmental glomerular sclerosis, systemic hypertension, and proteinuria at a young age. Micropuncture and morphological studies were performed in two inbred strains of fawn-hooded rats, FHH and FHL, with different susceptibilities to develop chronic renal failure. FHH rats have higher values for systolic blood pressure and proteinuria and more rapid development of focal and segmental glomerular sclerosis and subsequent chronic renal failure as compared with genetically closely related FHL rats. FHH and FHL strains and a Wistar control strain, WAG, were matched for age and were studied at 16 wk. FHH, FHL, and WAG-old (WAG-O) strains were matched for weight, and the last group was studied at 22 wk. WAG were also matched for weight to a young group of FHH rats (FHH-Y), and these were studied at 8 wk. In comparison with WAG and WAG-O rats, FHH and FHH-Y rats exhibited an increased in mean glomerular capillary hydraulic pressure (WAG, 52 +/- 1 mm Hg; WAG-O, 47 +/- 2 mm Hg; FHH, 60 +/- 2 mm Hg; FHH-Y, 65 +/- 1 mm Hg), whereas values in FHL animals were intermediate (56 +/- 2 mm Hg). No significant differences in glomerular volume were found among groups. Moderate focal and segmental glomerular sclerosis developed in FHH and FHH-Y rats, with values for older FHH rats being significantly greater than those for WAG, WAG-O, and FHL animals. Thus, the genetically determined sensitivity to develop proteinuria, focal and segmental glomerular sclerosis, and chronic renal failure in fawn-hooded rats correlated with early evidence of glomerular capillary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

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