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.

Influence of parathyroid hormone on glomerular ultrafiltration in the rat

1978 ◽  
Vol 234 (5) ◽  
pp. F393-F401
Author(s):  
I. Ichikawa ◽  
H. D. Humes ◽  
T. P. Dousa ◽  
B. M. Brenner
Keyword(s):  
Parathyroid Hormone ◽  
Flow Rate ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Hydraulic Pressure ◽  
Oncotic Pressure ◽  
Mean Values ◽  
Single Nephron Filtration Rate ◽  
Single Nephron ◽  
Glomerular Ultrafiltration

Experiments were performed on 22 plasma-expanded Munich-Wistar rats to investigated the effects of parathyroid hormone (PTH) on the determinants of glomerular ultrafiltration. Mean values for single nephron filtration rate (SNGFR), glomerular plasma flow rate (QA), systemic oncotic pressure, and transglomerular hydraulic pressure difference (deltaP) were similar in acutely thyroparathyroidectomized (TPTX) rats and non-TPTX rats. Nevertheless, the glomerular capillary ultrafiltration coefficient (Kf) was uniformly higher in TPTX rats (greater than 0.113 +/- 0.005 (SE) nl/(s.mmHg)] than in non-TPTX controls (0.088 +/- 0.005). In TPTX rats, infusion of a submaximal dose (1 U/kg per min) of PTH resulted in significant decreases in SNGFR at constant QA and deltaP, due primarily to return of Kf to non-TPTX levels. Infusion of 10 U/kg per min of PTH to non-TPTX rats further reduced Kf, on average to 0.042 +/- 0.001 nl/(s.mmHg), leading to further reduction in SNGFR, whereas QA and deltaP again remained constant. These findings suggest that PTH may play an important role in modulating Kf, and consequently, SNGFR.

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.

scholarly journals Induction of p27KIP1 after unilateral ureteral obstruction is independent of angiotensin II

2002 ◽  
Vol 61 (1) ◽  
pp. 68-79 ◽  
Author(s):  
Jens H. Gerth ◽  
Jörg Kriegsmann ◽  
T. Tong Trinh ◽  
Rolf A.K. Stahl ◽  
Thoralf Wendt ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction

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.

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.

Apoptosis of circulating lymphocyte in rats with unilateral ureteral obstruction: Role of angiotensin II

Nephrology ◽  
2005 ◽  
Vol 10 (5) ◽  
pp. 464-469 ◽  
Author(s):  
SOMCHIT EIAM-ONG ◽  
JANPEN UDOM ◽  
TADA SUEBLINVONG ◽  
SOMCHAI EIAM-ONG
Keyword(s):  
Angiotensin Ii ◽  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction

Angiotensin II control of the renal microcirculation in rats with reduced renal mass

1990 ◽  
Vol 258 (2) ◽  
pp. F414-F422 ◽  
Author(s):  
J. C. Pelayo ◽  
A. H. Quan ◽  
P. F. Shanley
Keyword(s):  
Renal Failure ◽  
Angiotensin Ii ◽  
Renal Mass ◽  
Wistar Rats ◽  
Sham Group ◽  
Ang Ii ◽  
Renal Ablation ◽  
Glomerular Hypertension ◽  
Single Nephron ◽  
Glomerular Ultrafiltration

It has been suggested that angiotensin II (ANG II) activation after renal ablation contributes to the altered glomerular dynamics and proteinuria that characterizes this model of chronic renal failure. In the present study, male Munich-Wistar rats underwent 75% renal ablation (Nx group). Two weeks later, micropuncture studies were performed in sham-operated rats (sham group) and Nx group rats during intravenous infusion of either a vehicle or two ANG II inhibitors, namely [Sar1, Ala8]ANG II or MK-421 administered at a rate of 0.3 and 1 mg.kg body wt-1.h-1, respectively. Acute ANG II inhibition in sham group had no effect on mean arterial pressure (MAP), glomerular dynamics, or proteinuria. In contrast, in Nx group ANG II inhibition lessened glomerular hypertension (from 64.7 +/- 1.0 to 55.4 +/- 1.7 mmHg, P less than 0.0001) the result of postglomerular vasodilation (P less than 0.01), normalized the glomerular ultrafiltration coefficient (from 0.038 +/- 0.002 to 0.005 +/- 0.002 nl.s-1.mmHg-1, P less than 0.0001), and attenuated proteinuria (from 42.1 +/- 6.5 to 28.1 +/- 5.4 micrograms/min, P less than 0.01). MAP, single-nephron GFR and plasma flow were unaffected. These results suggest that ANG II activity is enhanced in nephrectomy, contributing in a major way to altered glomerular dynamics and proteinuria.

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