Is the Glomerular Capillary Hydraulic Pressure Increased in Moderately Hyperglycemic Rats on Normal Protein Intake?1

2015 ◽  
pp. 18-26
Author(s):  
B. Prins ◽  
H. J. G. Bilo ◽  
A. J. M. Donker
Keyword(s):  
Protein Intake ◽  
Hydraulic Pressure ◽  
Glomerular Capillary

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.

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

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.

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)

scholarly journals Glomerular preload and afterload reduction as a tool to lower urinary protein leakage: will such treatments also help to improve renal function outcome?

1993 ◽  
Vol 3 (7) ◽  
pp. 1333-1341 ◽  
Author(s):  
P E de Jong ◽  
S Anderson ◽  
D de Zeeuw
Keyword(s):  
Ace Inhibitors ◽  
Dietary Protein ◽  
Protein Restriction ◽  
Urinary Protein ◽  
Hydraulic Pressure ◽  
Protein Loss ◽  
Afterload Reduction ◽  
Dietary Protein Restriction ◽  
Glomerular Capillary ◽  
Lower Urinary

It has been well documented that different therapeutic strategies, including angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs, and dietary protein restriction, lower urinary protein excretion in patients with diabetic and non-diabetic nephropathy. Experimental evidence suggests that this antiproteinuric effect is, at least in part, related to a reduction in the glomerular capillary hydraulic pressure. ACE inhibitors appear to achieve this reduction in glomerular capillary pressure, mainly through a fall in postglomerular arteriolar resistance, whereas dietary protein restriction and non-steroidal antiinflammatory drugs appear to invoke the response predominantly through an increase in preglomerular resistance. This leads to the suggestion that both "glomerular preload reduction" (afferent vasoconstriction) and "glomerular afterload reduction" (efferent vasodilation) will result in an anti-proteinuric response. Interestingly, these same therapeutic regimens, particularly the ACE inhibitors and low-protein diets, have been proven to prevent progressive glomerulosclerosis in animal models. This concept of influencing glomerular hemodynamics both at the afferent and efferent arteriolar level may open new perspectives in the treatment of patients with renal protein loss and renal failure. At present, however, it is too early to conclude whether the fall in proteinuria induced by these treatments will also contribute to a better renal survival of these patients.

Which Method Should Be Used to Assess Protein Intake in Peritoneal Dialysis Patients? Assessment of Agreement Between Protein Equivalent of Total Nitrogen Appearance and 24-Hour Dietary Recall

2020 ◽  
Author(s):  
Maryanne Zilli Canedo Silva ◽  
Barbara Perez Vogt ◽  
Nayrana Soares Carmo Reis ◽  
Rogerio Carvalho Oliveira ◽  
Jacqueline Costa Teixeira Caramori
Keyword(s):  
Peritoneal Dialysis ◽  
Total Nitrogen ◽  
Protein Intake ◽  
Dialysis Patients ◽  
Dietary Recall
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