Determination of Renal Plasma Flow by Endogenous Hippuric Acid Clearance in the Conscious Rat

Author(s):  
Eva Baunack ◽  
Klaus G�rtner
1996 ◽  
Vol 23 (4) ◽  
pp. 365-370 ◽  
Author(s):  
Michel Stoffel ◽  
François Jamar ◽  
Chris Van Nerom ◽  
Alfons Verbruggen ◽  
Tatiana Besse ◽  
...  

1989 ◽  
Vol 10 (2) ◽  
pp. 99-108 ◽  
Author(s):  
HUSSEIN M. ABDEL-DAYEM ◽  
SAMY SADEK ◽  
RIAD AL-BAHAR ◽  
MOHAMMED SABHA ◽  
MOHAMMAD EL-SAYED

1990 ◽  
Vol 68 (4) ◽  
pp. 500-504 ◽  
Author(s):  
Ravi D. Kaushal ◽  
Thomas W. Wilson

We had previously shown that selective thromboxane synthetase inhibition with furegrelate increases urinary excretion of 6-ketoPGF1α, the hydrolysis product of prostacyclin after stimulation of renal prostaglandin synthesis with furosemide. The present study assessed the functional significance of this "redirection" of prostaglandin formation using a more physiologic stimulus, angiotensin II. Sprague–Dawley rats (n = 27) were fitted with a transabdominal bladder cannula. Five days later they were given angiotensin II (10 mg∙kg−1∙min−1) by intravenous infusion. After 30 min, an infusion of furegrelate, 2 mg/kg, then 2 mg∙kg−1∙h−1, (n = 9); indomethacin, 2 mg/kg, then 2 mg∙kg−1∙h−1 (n = 9); or vehicle, 250 μL, then 0.018 mL/min (n = 9) was begun for 60 min. Clearance of [14C]para-aminohippuric acid was taken as a measure of renal plasma flow. Angiotensin II raised the mean arterial pressure in all groups. Administration of furegrelate or indomethacin did not change mean arterial pressure or heart rate. Angiotensin II reduced [14C]p-aminohippuric acid clearance by about 32% (1.42 ± 0.18 to 0.97 ± 0.07 mL∙min−1∙100 g−1, p < 0.05). Furegrelate attenuated this renal vasoconstriction (0.97 ± 0.07 to 1.38 ± 0.17 mL∙min−1∙100 g−1, p < 0.05), while indomethacin increased it by a further 32% (1.78 ± 0.12 to 1.20 ± 0.12 mL∙min−1∙100 g−1, p < 0.05). Vehicle alone had no effect. Furegrelate reduced serum thromboxane B2 by 90% (6.52 ± 0.030 to 0.7 ± 0.21 ng/100 μL, p < 0.05), while indomethacin reduced it by 73% (5.9 ± 0.99 to 1.4 ± 0.20 ng/100 μL, p < 0.05). We conclude that furegrelate attenuates the renal vasoconstriction of angiotensin II, presumably by enhancing the formation of vasodilator prostaglandins.Key words: angiotensin II, furegrelate, indomethacin, para-aminohippuric acid clearance.


1960 ◽  
Vol 198 (5) ◽  
pp. 1044-1048 ◽  
Author(s):  
G. S. Kanter

The purpose of this study was to investigate the factors that determine the direction and magnitude of the alteration in GFR (glomerular filtration rate) and RPF (renal plasma flow) in hyperthermia. The investigation was conducted on anesthetized dogs. Creatinine clearance was used as a measure of GFR and para-aminohippuric acid clearance was used as a measure of RPF. The GFR in 12 mildly dehydrated dogs went from a control value of 68.4 ± 4.5 ml/min. at RT (rectal temperature) of 38.9°C to a GFR of 25.1 ± 8.5 ml/min. at a RT of 42.1°C at the end of 5 hours of exposure to heat. Final dehydration averaged –2.0% body weight. The fall in GFR and RPF was not due to dehydration for in a group of six hydrated dogs (+4% body wt. at end) similar results were obtained. No decrease in GFR or RPF occurred in either hydrated or dehydrated dogs until severe hyperthermia (> 41.2°C) was present. Though there was a decline in blood pressure towards the end of each experiment, in both groups, the decrease in GFR and RPF preceded any marked fall in pressure. Both groups showed an increase in hematocrit and a decrease in plasma volume (measured by T-1824 dilution) which became marked at the end of 5 hours of exposure to heat. The decrease in GFR and RPF appears directly related to the hyperthermia for upon rapid cooling GFR and RPF increases towards normal in spite of the persisting decreased blood pressure and plasma volume and increased hematocrit.


1992 ◽  
Vol 13 (1) ◽  
pp. 379
Author(s):  
T. Aburano ◽  
N. Shuke ◽  
T. Takayama ◽  
K. Yokoyama ◽  
T. Michigishi ◽  
...  

1986 ◽  
Vol 11 (11) ◽  
pp. 758-759
Author(s):  
JOHN L. FLOYD ◽  
DONALD E. JACKSON ◽  
JIM M. THOMAS

1999 ◽  
Vol 277 (2) ◽  
pp. F312-F318 ◽  
Author(s):  
Geraldine Corrigan ◽  
Deepa Ramaswamy ◽  
Osun Kwon ◽  
F. Graham Sommer ◽  
Edward J. Alfrey ◽  
...  

We determined the effect of postischemic injury to the human renal allograft on p-aminohippurate (PAH) extraction (EPAH) and renal blood flow. We evaluated renal function in 44 allograft recipients on two occasions: 1–3 h after reperfusion ( day 0) and again on postoperative day 7. On day 0 subsets underwent intraoperative determination of renal blood flow ( n = 35) by Doppler flow meter and EPAH( n = 25) by renal venous assay. Blood flow was also determined in another subset of 16 recipients on postoperative day 7 by phase contrast-cine-magnetic resonance imaging, and EPAH was computed from the simultaneous PAH clearance. Glomerular filtration rate (GFR) on day 7 was used to divide subjects into recovering ( n = 23) and sustained ( n = 21) acute renal failure (ARF) groups, respectively. Despite profound depression of GFR in the sustained ARF group, renal plasma flow was only slightly depressed, averaging 296 ± 162 ml ⋅ min−1 ⋅ 1.73 m−2 on day 0 and 202 ± 72 ml ⋅ min−1 ⋅ 1.73 m−2 on day 7, respectively. These values did not differ from corresponding values in the recovering ARF group: 252 ± 133 and 280 ± 109 ml ⋅ min−1 ⋅ 1.73 m−2, respectively. EPAH was profoundly depressed on day 0, averaging 18 ± 14 and 10 ± 7% in recovering and sustained ARF groups, respectively, vs. 86 ± 6% in normal controls ( P < 0.001). Corresponding values on day 7remained significantly depressed at 65 ± 20 and 11 ± 22%, respectively. We conclude that postischemic injury to the renal allograft results in profound impairment of EPAH that persists for at least 7 days, even after the onset of recovery. An ensuing reduction in urinary PAH clearance results in a gross underestimate of renal plasma flow, which is close to the normal range in the initiation, maintenance, and recovery stages of this injury.


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