The Isolated Perfused Rat Kidney: Filtering and Non-Filtering Models in the Assessment of Altered Renal Vascular Resistance in Nephrotoxicity

1989 ◽  
pp. 659-662 ◽  
Author(s):  
Peter Ratcliffe ◽  
Zoltan Endre ◽  
Lynn Nicholls ◽  
John Tange ◽  
John Ledingham
Keyword(s):  
Vascular Resistance ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Renal Vascular

scholarly journals Effects of cyclosporine and its metabolites in the isolated perfused rat kidney.

1993 ◽  
Vol 4 (2) ◽  
pp. 168-177
Author(s):  
K A Roby ◽  
L M Shaw
Keyword(s):  
Vascular Resistance ◽  
Rat Kidney ◽  
Parent Drug ◽  
Renal Vascular Resistance ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Before And After ◽  
Vascular Obstruction ◽  
Dose Responses ◽  
Renal Vascular

The isolated perfused rat kidney (IPK) was used to study the acute effects of cyclosporin A (CsA) and its metabolites (M1, M17, M18, M21 and M-COOH). GFR, renal vascular resistance, and sodium, potassium and water reabsorption were measured before and after the addition of CsA/metabolites/vehicles. There was no difference in CsA effect (mild decrease in GFR and increase in renal vascular resistance with the inclusion of plasma (10 mL) or whole blood (20 mL) in the albumin perfusate (120 mL). Intralipid was used as the vehicle for CsA and the metabolites because methanol, ethanol, and Cremophor had significant effects on GFR. Intralipid enhanced the effect of CsA 25-fold, giving CsA dose responses comparable to those of human kidneys. This enhanced effect with intralipid was due to vasoconstriction, not vascular obstruction, and was apparently specific to CsA (no enhancement of norepinephrine with Intralipid). The primary metabolites (M1, M17, and M21) caused decreases in GFR comparable to or slightly less than those caused by CsA. The secondary metabolites (M18 and M-COOH) caused more modest declines in GFR. Cyclosporine metabolite levels in patient blood often greatly exceed levels of the parent drug; these studies suggest that the metabolites may contribute significantly to CsA nephrotoxicity in patients.

Inhibition by bradykinin of renal adrenergic effects in anesthetized rats

1984 ◽  
Vol 246 (4) ◽  
pp. F387-F394
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitors ◽  
Renal Nerve ◽  
Anesthetized Rats ◽  
Renal Vascular

We studied the contribution of prostaglandins to the actions of bradykinin at the renal vascular adrenergic neuroeffector junction by examining the effect of the peptide on the decrease in renal blood flow elicited by renal nerve stimulation and injected norepinephrine in pentobarbital-anesthetized rats with or without pretreatment with the cyclooxygenase inhibitors sodium meclofenamate or indomethacin. Infusion of bradykinin, 10 ng X kg-1 X min-1, into the renal artery reduced both the basal and the rise in renal vascular resistance produced by nerve stimulation or norepinephrine. The prostaglandin precursor arachidonic acid, 5 micrograms X kg-1 X min-1, infused into the renal artery, also reduced renal vascular resistance and the vasoconstrictor response elicited by either adrenergic stimulus. In animals pretreated with either sodium meclofenamate or indomethacin, the effect of arachidonic acid, but not that of bradykinin, to produce renal vasodilation and to attenuate adrenergically induced renal vasoconstriction was abolished. These data suggest that bradykinin produces renal vasodilation and inhibits the renal vasoconstrictor effect of adrenergic stimuli in the rat kidney in vivo by a mechanism unrelated to prostaglandin synthesis.

Renal vascular responses of kinins in the isolated perfused rat kidney

1997 ◽  
Vol 15 (11) ◽  
pp. 1349
Author(s):  
K Bagate ◽  
L Dévélioglu ◽  
B Michel ◽  
M Grima ◽  
J-L Imbs ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Vascular Responses ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Renal Vascular

Renal Vasoconstriction in Glycerol-Induced Acute Renal Failure. Studies in the Isolated Perfused Rat Kidney

1978 ◽  
Vol 55 (3) ◽  
pp. 249-252
Author(s):  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
A. Konrads ◽  
F. Gross
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Vascular Resistance ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Renin Release ◽  
Pass System ◽  
Renal Vasoconstriction ◽  
Renal Vascular

1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l, 10 ml/kg). Either 2 or 4–6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mmHg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra-rather than intra-renal mechanisms.

Effect of Polycations on the Function of the Isolated Perfused Rat Kidney

1990 ◽  
Vol 79 (6) ◽  
pp. 591-598 ◽  
Author(s):  
J. D. Firth
Keyword(s):  
Molecular Weight ◽  
Vascular Resistance ◽  
Filtration Rate ◽  
Rat Kidney ◽  
Minimal Change Nephrotic Syndrome ◽  
High Concentration ◽  
Heavy Proteinuria ◽  
Isolated Perfused Rat Kidney ◽  
Filtration Barrier ◽  
Perfused Rat Kidney

1. In minimal change nephrotic syndrome the occurrence of heavy proteinuria can be explained on the basis of a reduction in charge selectivity of the glomerular filtration barrier, and it has been proposed that this might be caused by the neutralization of anionic groups by a circulating polycationic factor. 2. The effects of two polycations, protamine and poly-l-lysine, on the function of the isolated perfused rat kidney have been examined. 3. Poly-l-lysine polymers of relatively high molecular weight (8800 and 17800) induced heavy proteinuria, while simultaneously causing a marked increase in renal vascular resistance and a fall in filtration rate. Protamine (approximate molecular weight 7000) at relatively high concentration induced modest proteinuria in the absence of effects on vascular resistance or filtration rate. 4. A poly-l-lysine polymer of lower molecular weight (3800) did not induce proteinuria. Protamine at a concentration of 40 μg/ml and below did not affect protein excretion either. Both provoked substantial natriuresis. This appeared to be largely due to an effect on the tubular handling of sodium since the filtration rate remained steady while fractional sodium excretion rose markedly. 5. The natriuretic effect of protamine was blocked by heparin, but not by indomethacin or verapamil, suggesting that the mechanism of natriuresis did not depend upon either prostaglandin production or entry of calcium through verapamil-sensitive channels.

The effect of sodium iothalamate on the vascular resistance of the isolated perfused rat kidney

1991 ◽  
Vol 64 (757) ◽  
pp. 50-54 ◽  
Author(s):  
J. L. Haylor ◽  
A. A. El Sayed ◽  
A. M. EI Nahas ◽  
S. K. Morcos
Keyword(s):  
Vascular Resistance ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney

Validation of a toxicity testing model by evaluating oxygen supply and energy state in the isolated perfused rat kidney

1991 ◽  
Vol 25 (3) ◽  
pp. 195-204 ◽  
Author(s):  
Takano Takehito ◽  
Nakata Kazuyo ◽  
Kawakami Tsuyoshi ◽  
Miyazaki Yoshifumi ◽  
Murakami Masataka ◽  
...  
Keyword(s):  
Oxygen Supply ◽  
Energy State ◽  
Rat Kidney ◽  
Toxicity Testing ◽  
Testing Model ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney
Sign in / Sign up

Export Citation Format

Share Document