Diuretic and hemodynamic effects of furosemide in the isolated dog kidney

1973 ◽  
Vol 277 (1) ◽  
pp. 13-26 ◽  
Author(s):  
N. T. Stowe ◽  
L. F. Wolterink ◽  
A. E. Lewis ◽  
J. B. Hook
Keyword(s):  
Hemodynamic Effects ◽  
Dog Kidney ◽  
Isolated Dog Kidney

Effect of an angiotensin II antagonist on autoregulation in the isolated dog kidney

1976 ◽  
Vol 230 (4) ◽  
pp. 1078-1083 ◽  
Author(s):  
GJ Kaloyanides ◽  
GF DiBona
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Flow Distribution ◽  
Renin Angiotensin System ◽  
Vascular Effects ◽  
Isolated Kidney ◽  
Angiotensin Ii Antagonist ◽  
Dog Kidney ◽  
Isolated Dog Kidney

The effect of the specific angiotensin II antagonist (AIIA), [1-sarcosine-8-alanine]angiotensin II, on autoregulation of glomerular filtration rate (GFR) and renal blood flow (RBF) in an isolated dog kidney was examined. Infusing the AIIA into the renal artery at 1.9 mug/min inhibited the renal vasoconstrictor action of angiotension II infused simultaneously at 1.15 mug/min. Under conditions of constant renal arterial pressure the AIIA had no significant effect on sodium excretion, GFR, RBF, cortical blood flow distribution (microsphere method), or renin secretion in non-renin-depleted kidneys. Similarly, no agonist properties were observed when the AIIA was infused into renin-depleted kidneys. This dose of the AIIA did not impair the capacity of the isolated kidney to regulate GFR or RBF when renal arterial pressure was increased from 100 to 150 mmHg. Efficiency of autoregulation of GFR and RBF was 77 and 82% of that predicted for perfect autoregulation. These values are not significantly different from those of the isolated kidney not infused with the antagonist. It is concluded that the angiotensin II antagonist, [1-sarcosine-8-alanine]angiotensin II, has no significant agonist properties, that it antagonizes the renal vascular effects of exogenously administered angiotensin II, but does not impair renal autoregulation. These data provide no support for the hypothesis that the renin-angiotensin system mediates the autoregulation of GFR and RBF.

Interactions between furosemide and vasopressin on hemodynamics and on water excretion by the isolated dog kidney

1976 ◽  
Vol 362 (3) ◽  
pp. 265-270 ◽  
Author(s):  
J. -L. Vanherweghem ◽  
J. Ducobu ◽  
A. D'hollander ◽  
C. Toussaint
Keyword(s):  
Water Excretion ◽  
Dog Kidney ◽  
Isolated Dog Kidney

Stimulation of glutamine metabolism by the antiepileptic drug, sodium valproate, in isolated dog kidney tubules

1989 ◽  
Vol 38 (22) ◽  
pp. 3947-3952 ◽  
Author(s):  
Guy Martin ◽  
Christian Michoudet ◽  
Gabriel Baverel
Keyword(s):  
Antiepileptic Drug ◽  
Sodium Valproate ◽  
Glutamine Metabolism ◽  
Kidney Tubules ◽  
Dog Kidney ◽  
Isolated Dog Kidney ◽  
Stimulation Of

Effects of indomethacin on renal hemodynamics and on water and sodium excretion by the isolated dog kidney

1975 ◽  
Vol 357 (3-4) ◽  
pp. 243-252 ◽  
Author(s):  
J. L. Vanherweghem ◽  
J. Ducobu ◽  
A. D'Hollander
Keyword(s):  
Sodium Excretion ◽  
Renal Hemodynamics ◽  
Dog Kidney ◽  
Water And Sodium Excretion ◽  
Isolated Dog Kidney

Effects of Endotoxin on Hemodynamics of Isolated Dog Kidney

1987 ◽  
pp. 81-85 ◽  
Author(s):  
Nadine Bourgeois ◽  
Charles Reuse ◽  
Jean-Marie Boeynaems ◽  
Michel Staroukine ◽  
Jean-Louis Vanherweghem
Keyword(s):  
Dog Kidney ◽  
Isolated Dog Kidney

Control by insulin of sodium potassium and water excretion by the isolated dog kidney

1971 ◽  
Vol 323 (1) ◽  
pp. 11-20 ◽  
Author(s):  
A. Nizet ◽  
P. Lefebvre ◽  
J. Crabb�
Keyword(s):  
Sodium Potassium ◽  
Water Excretion ◽  
Dog Kidney ◽  
Isolated Dog Kidney

Vasodilator Properties of Ethacrynic Acid in the Perfused Dog Kidney

1970 ◽  
Vol 38 (3) ◽  
pp. 347-357 ◽  
Author(s):  
R. G. Dluhy ◽  
G. L. Wolf ◽  
D. P. Lauler
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Body Fluid ◽  
Ethacrynic Acid ◽  
Volume Depletion ◽  
Dog Kidney ◽  
Renal Vascular ◽  
Isolated Dog Kidney ◽  
Acid Administration

1. Ethacrynic acid reduces renal vascular resistance of the isolated dog kidney. 2. Ethacrynic acid induced natriuresis can occur despite stabilization of renal blood flow, but augmentation of blood flow increases the natriuretic response. 3. Vasodilatation and natriuresis after ethacrynic acid administration occurred together in time and were not separable. The onset and peak natriuretic and vasodilator responses frequently coincided in time. 4. Ethacrynic acid induced vasodilatation could be inhibited by loss of body fluid. The rise in resistance could be avoided by adequate volume replacement and by prevention of volume depletion.

scholarly journals Stimulation of glutamine metabolism by 3-aminopicolinate in isolated dog kidney-cortex tubules

1983 ◽  
Vol 210 (2) ◽  
pp. 483-487 ◽  
Author(s):  
D Durozard ◽  
G Baverel
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Glutamine Metabolism ◽  
Kidney Cortex ◽  
Kidney Tubules ◽  
Direct Stimulation ◽  
Dog Kidney ◽  
Glucose Synthesis ◽  
Isolated Dog Kidney ◽  
Gluconeogenic Substrates ◽  
Stimulation Of

1. The effects of 3-aminopicolinate, a known hyperglycaemic agent in the rat, on glutamine metabolism were studied in isolated dog kidney tubules. 2. 3-Aminopicolinate greatly stimulated glutamine (but not glutamate) removal and glutamate accumulation from glutamine as well as formation of ammonia, aspartate, lactate, alanine and glucose. 3. The increased accumulation of aspartate from glutamine and glutamate, and the inhibition of glucose synthesis from various non-nitrogenous gluconeogenic substrates, as well as the increased accumulation of malate from succinate, support the proposal that 3-aminopicolinate is an inhibitor rather than a stimulator of phosphoenolpyruvate carboxykinase (EC 4.1.1.32) in dog kidney tubules. 4. With glutamine as substrate, the increase in flux through glutamate dehydrogenase (EC 1.4.1.3) could not explain the large increase in glutamine removal caused by 3-aminopicolinate. 5. Inhibition by amino-oxyacetate of accumulation of aspartate and alanine from glutamine caused by 3-aminopicolinate did not prevent the acceleration of glutamine utilization. 6. These data are consistent with a direct stimulation of glutaminase (EC 3.5.1.2) by 3-aminopicolinate in dog kidney tubules.

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