Pressure-dependent action of angiotensin II on glomerular filtration in the isolated rat kidney

1982 ◽  
Vol 60 (10) ◽  
pp. 1311-1314 ◽  
Author(s):  
Thomas H. Steele ◽  
Jeanne H. Gottstein ◽  
Laura Challoner-Hue
Keyword(s):  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Rat Kidney ◽  
Sodium Concentration ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Urine Sodium ◽  
Isolated Rat Kidney ◽  
Isolated Rat

We examined the action of angiotensin II (AII) on isolated rat kidney perfused with a recirculating cell-free solution at either 12 pKa (90 mmHg) or 17 kPa (128 mmHg). The renal perfusion pressure was maintained constant while sufficient All was added to increase the renal vascular resistance by 50%. In the low-pressure kidneys, AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. In the high-pressure kidneys, GFR initially was significantly greater but was not affected by AII. In these experiments, AII had no effect on sodium reabsorption or excretion and decreased the urine sodium concentration by 7%. The data suggest that AII could be involved in autoregulation of the GFR without producing large changes in sodium excretion.

Inhibition of Renin Secretion in the Isolated Rat Kidney by Antidiuretic Hormone

1975 ◽  
Vol 49 (1) ◽  
pp. 73-76 ◽  
Author(s):  
R. Vandongen
Keyword(s):  
Antidiuretic Hormone ◽  
Calcium Ions ◽  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. The effect of antidiuretic hormone (ADH) on isoprenaline-stimulated renin secretion was examined in the isolated rat kidney perfused with modified Krebs-Ringer saline. 2. Intrarenal infusion of ADH effectively prevented stimulation of renin secretion by isoprenaline whilst increasing renal perfusion pressure. 3. The exclusion of calcium ions from the perfusion medium abolished the vasoconstrictor effect of ADH and attenuated the inhibitory effect of ADH on isoprenaline-stimulated renin secretion. However, significant suppression of renin secretion was still apparent compared with experiments where isoprenaline was infused alone. 4. These observations indicate that ADH inhibits renin secretion and that this is effected by a direct action on the kidney. Although this may be partly mediated by the rise in renal perfusion pressure, an additional direct effect of ADH on the renin-producing cell, which is dependent on the availability of calcium ions, is proposed.

Inhibition of distal tubular sodium reabsorption by angiotensin II

1963 ◽  
Vol 205 (1) ◽  
pp. 133-138 ◽  
Author(s):  
Arthur J. Vander
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Sodium Concentration ◽  
Relative Increase ◽  
Sodium Reabsorption ◽  
Left Renal Artery ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular ◽  
The Right ◽  
Stop Flow

Angiotensin II or norepinephrine was infused directly into the left renal artery of anesthetized dogs undergoing mannitol diuresis, and the right and left kidneys were compared for GFR (Ccr or Cin), RPF (Cpah), sodium excretion, and distal stop-flow sodium and inulin patterns. Both angiotensin and norepinephrine caused similar reductions of GFR and RPF on the left, as compared with the right, but only angiotensin prevented normal lowering of left distal stop-flow sodium concentration, even when length of occlusion was 14 min. The minimum effective dose was 6–12 mµg/kg min, and maximal differences between left and right sodium minima occurred with 50 mµg/kg min. Distal inulin patterns were not altered by angiotensin, nor were "postocclusive" inulin patterns. Clearance data demonstrated that when GFR changes were taken into account angiotensin caused a relative increase in sodium excretion compared to control or norepinephrine-infused dogs. These stop-flow and clearance data support the hypothesis that angiotensin inhibits distal sodium reabsorption by a direct tubular effect. No attempt was made to evaluate possible effects of angiotensin on proximal tubular sodium reabsorption.

scholarly journals Effects of angiotensin II on the renal excretion of urodilatin in the isolated rat kidney

Critical Care ◽  
10.1186/cc894 ◽  
2000 ◽  
Vol 4 (Suppl 1) ◽  
pp. P174
Author(s):  
M Heringlake ◽  
K Wagner ◽  
L Bahlmann ◽  
S Klaus ◽  
J Schumacher ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Excretion ◽  
Rat Kidney ◽  
Isolated Rat Kidney ◽  
Isolated Rat

Characterization of Ascorbic Acid Uptake by Isolated Rat Kidney Cells

1991 ◽  
Vol 121 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Delores M. Bowers-Komro ◽  
Donald B. McCormick
Keyword(s):  
Ascorbic Acid ◽  
Rat Kidney ◽  
Acid Uptake ◽  
Kidney Cells ◽  
Isolated Rat Kidney ◽  
Isolated Rat

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

Toxicity of depleted uranium on isolated rat kidney mitochondria

2012 ◽  
Vol 1820 (12) ◽  
pp. 1940-1950 ◽  
Author(s):  
Fatemeh Shaki ◽  
Mir-Jamal Hosseini ◽  
Mahmoud Ghazi-Khansari ◽  
Jalal Pourahmad
Keyword(s):  
Rat Kidney ◽  
Depleted Uranium ◽  
Kidney Mitochondria ◽  
Isolated Rat Kidney ◽  
Isolated Rat
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