STUDIES OF THE EFFECT OF LARGE DOSES OF BACTERIAL PYROGEN IN THE DOG: 2. AN EXPLANATION FOR THE URINE DILUTION

1963 ◽  
Vol 41 (5) ◽  
pp. 1317-1324 ◽  
Author(s):  
J. Leonard Brandt ◽  
Ignatios J. Voudoukis ◽  
James Harrop
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Concentration ◽  
Paired Control ◽  
Bacterial Pyrogen ◽  
Renal Cortical Tissue ◽  
Solute Excretion ◽  
Counter Current ◽  
Tissue Sodium ◽  
Total Renal Blood Flow

Previous studies with large IV doses of bacterial endotoxin in dogs have shown this material to cause a diuresis which is uniformly associated with a rise in total renal blood flow, increased solute excretion, and a fall in Uosm unresponsive to ADH. The present study has demonstrated that renal cortical tissue sodium concentration is unaffected by endotoxin whereas renal sodium concentration of outer and inner medullary portions showed a striking fall. Endotoxin-treated kidneys were compared to their respective paired control (no endotoxin). It is postulated that the rise in total renal blood flow, following endotoxin, is mainly medullary and causes a washout of medullary interstitium multiplier deposited sodium. The efficiency of the renal counter current exchanger is impaired and tubule to interstitium gradient reduced. This would account for observed falls in Uosm and relative unresponsiveness to ADH after endotoxin.

STUDIES OF THE EFFECT OF LARGE DOSES OF BACTERIAL PYROGEN IN THE DOG: 2. AN EXPLANATION FOR THE URINE DILUTION

1963 ◽  
Vol 41 (1) ◽  
pp. 1317-1324
Author(s):  
J. Leonard Brandt ◽  
Ignatios J. Voudoukis ◽  
James Harrop
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Concentration ◽  
Paired Control ◽  
Bacterial Pyrogen ◽  
Renal Cortical Tissue ◽  
Solute Excretion ◽  
Counter Current ◽  
Tissue Sodium ◽  
Total Renal Blood Flow

Previous studies with large IV doses of bacterial endotoxin in dogs have shown this material to cause a diuresis which is uniformly associated with a rise in total renal blood flow, increased solute excretion, and a fall in Uosm unresponsive to ADH. The present study has demonstrated that renal cortical tissue sodium concentration is unaffected by endotoxin whereas renal sodium concentration of outer and inner medullary portions showed a striking fall. Endotoxin-treated kidneys were compared to their respective paired control (no endotoxin). It is postulated that the rise in total renal blood flow, following endotoxin, is mainly medullary and causes a washout of medullary interstitium multiplier deposited sodium. The efficiency of the renal counter current exchanger is impaired and tubule to interstitium gradient reduced. This would account for observed falls in Uosm and relative unresponsiveness to ADH after endotoxin.

Measurement of Intrarenal Blood-Flow Distribution in the Rabbit Using Radioactive Microspheres

1975 ◽  
Vol 48 (1) ◽  
pp. 51-60 ◽  
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Flow Distribution ◽  
Rabbit Kidney ◽  
Radioactive Microspheres ◽  
Injection Dose ◽  
Intrarenal Blood Flow ◽  
Total Renal Blood Flow

1. Total renal blood flow and its distribution within the renal cortex of the conscious rabbit were studied with radioactive microspheres of 15 and 25 μm diameter. 2. The reliability of the microsphere technique was influenced by microsphere diameter and number (dose). The optimum microsphere diameter for determination of flow distribution in the rabbit kidney was 15 μm and dose 100–150 000 spheres. 3. Spheres of 15 μm nominal diameter were randomly distributed within the renal cortex of adult rabbits. The larger spheres in batches nominally 15 μm in diameter in young rabbits and 25 μm diameter in adult rabbits were preferentially distributed to the superficial cortex. 4. In adult rabbits 15 μm diameter spheres lodged in glomerular capillaries. Larger spheres occasionally lodged in interlobular arteries causing intrarenal haemorrhage. 5. Microspheres of 15 μm caused a decrease in renal clearance of creatinine and of p-aminohippurate when the total injection dose was about 200 000 spheres. These effects were greater when the injection dose was increased to 500 000 spheres. 6. The reduction in total renal blood flow observed with large doses of spheres largely reflected decreased outer cortical flow, as measured by a second injection of spheres, and confirmed by a decrease in p-aminohippurate extraction. 7. The reproducibility of multiple injection studies was limited by these intrarenal effects of microspheres. 8. Total renal blood flow measured in six rabbits in acute experiments by the microsphere technique was 107 ± 12 (mean±sd) ml/min and by p-aminohippurate clearance was 100 ± 10 ml/min. 9. Total renal blood flow in twelve conscious, chronically instrumented rabbits was 125 ± 11 ml/min, of which 92 ± 6 ml/min was distributed to the superficial cortex and 33 ± 4 ml/min to the deep cortex.

Aortic blood flow subtraction: an alternative method for measuring total renal blood flow in conscious dogs

2002 ◽  
Vol 282 (5) ◽  
pp. R1528-R1535 ◽  
Author(s):  
N. C. F. Sandgaard ◽  
J. L. Andersen ◽  
N.-H. Holstein-Rathlou ◽  
P. Bie
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Aortic Blood Flow ◽  
Excretory Function ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Bilateral Carotid ◽  
Total Renal Blood Flow

We have measured total renal blood flow (TRBF) as the difference between signals from ultrasound flow probes implanted around the aorta above and below the renal arteries. The repeatability of the method was investigated by repeated, continuous infusions of angiotensin II and endothelin-1 seven times over 8 wk in the same dog. Angiotensin II decreased TRBF (350 ± 16 to 299 ± 15 ml/min), an effect completely blocked by candesartan (TRBF 377 ± 17 ml/min). Subsequent endothelin-1 infusion reduced TRBF to 268 ± 20 ml/min. Bilateral carotid occlusion (8 sessions in 3 dogs) increased arterial blood pressure by 49% and decreased TRBF by 12%, providing an increase in renal vascular resistance of 69%. Dynamic analysis showed autoregulation of renal blood flow in the frequency range <0.06–0.07 Hz, with a peak in the transfer function at 0.03 Hz. It is concluded that continuous measurement of TRBF by aortic blood flow subtraction is a practical and reliable method that allows direct comparison of excretory function and renal blood flow from two kidneys. The method also allows direct comparison between TRBF and flow in the caudal aorta.

Role of the renal medulla in volume and arterial pressure regulation

1997 ◽  
Vol 273 (1) ◽  
pp. R1-R15 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Fluid Pressure ◽  
Regulatory System ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vasa Recta ◽  
Pressure Natriuresis ◽  
Total Renal Blood Flow

The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W., N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named "hormones," importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.

scholarly journals Renal hemodynamics and fatty acid uptake: effects of obesity and weight loss

2019 ◽  
Vol 317 (5) ◽  
pp. E871-E878 ◽  
Author(s):  
Eleni Rebelos ◽  
Prince Dadson ◽  
Vesa Oikonen ◽  
Hidehiro Iida ◽  
Jarna C. Hannukainen ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Weight Loss ◽  
Blood Flow ◽  
Cardiac Output ◽  
Fatty Acid ◽  
Renal Blood Flow ◽  
Renal Hemodynamics ◽  
Renal Volume ◽  
Obese Subjects ◽  
Total Renal Blood Flow

Human studies of renal hemodynamics and metabolism in obesity are insufficient. We hypothesized that renal perfusion and renal free fatty acid (FFA) uptake are higher in subjects with morbid obesity compared with lean subjects and that they both decrease after bariatric surgery. Cortical and medullary hemodynamics and metabolism were measured in 23 morbidly obese women and 15 age- and sex-matched nonobese controls by PET scanning of [15O]-H2O (perfusion) and 14( R,S)-[18F]fluoro-6-thia-heptadecanoate (FFA uptake). Kidney volume and radiodensity were measured by computed tomography, cardiac output by MRI. Obese subjects were re-studied 6 mo after bariatric surgery. Obese subjects had higher renal volume but lower radiodensity, suggesting accumulation of water and/or lipid. Both cardiac output and estimated glomerular filtration rate (eGFR) were increased by ~25% in the obese. Total renal blood flow was higher in the obese [885 (317) (expressed as median and interquartile range) vs. 749 (300) (expressed as means and SD) ml/min of controls, P = 0.049]. In both groups, regional blood perfusion was higher in the cortex than medulla; in either region, FFA uptake was ~50% higher in the obese as a consequence of higher circulating FFA levels. Following weight loss (26 ± 8 kg), total renal blood flow was reduced ( P = 0.006). Renal volume, eGFR, cortical and medullary FFA uptake were decreased but not fully normalized. Obesity is associated with renal structural, hemodynamic, and metabolic changes. Six months after bariatric surgery, the hemodynamic changes are reversed and the structural changes are improved. On the contrary, renal FFA uptake remains increased, driven by high substrate availability.

Renal Vascular Response to Haemorrhage in the Rabbit after Pentobarbitone, Chloralose–Urethane and Ether Anaesthesia

1978 ◽  
Vol 54 (5) ◽  
pp. 489-494
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Ether Anaesthesia ◽  
Before And After ◽  
Conscious Rabbits ◽  
Urethane Anaesthesia ◽  
Renal Vascular ◽  
Cortical Distribution ◽  
Total Renal Blood Flow

1. Total renal blood flow and its cortical distribution were measured by the microsphere technique before and after haemorrhage in conscious rabbits, and after haemorrhage in rabbits anaesthetized with pentobarbitone, chloralose—urethane or ether. 2. The average blood loss necessary to achieve a fall in systolic blood pressure to about 65 mmHg was 101 ml in conscious rabbits and 38, 90 and 118 ml in weight-matched groups of rabbits anaesthetized with pentobarbitone, chloralose—urethane and ether respectively. 3. After haemorrhage in conscious rabbits total renal blood flow fell by 25%, this fall being confined to the superficial renal cortex. 4. In rabbits subject to haemorrhage under pentobarbitone anaesthesia renal blood flow fell by a further 23% when compared with the conscious bled rabbits. This reduction in blood flow was confined to the superficial cortex. 5. Haemorrhage in the rabbits subjected to chloralose—urethane anaesthesia caused no significant change in renal blood flow, as compared with conscious bled rabbits. 6. Haemorrhage under ether anaesthesia was associated with a further 33% fall in total renal blood flow, as compared with conscious bled rabbits. This was associated with a fall of 32% and 34% in superficial and deep cortical blood flow respectively. 7. Animals subjected to general anaesthesia may be particularly susceptible to the renal haemodynamic effects of haemorrhage.

Alteration of canine renal vascular response to hemorrhage by inhibitors of prostaglandin synthesis

1976 ◽  
Vol 230 (4) ◽  
pp. 940-945 ◽  
Author(s):  
JL Data ◽  
LC Chang ◽  
AS Nies
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Control Period ◽  
Prostaglandin Synthesis ◽  
Hemorrhagic Hypotension ◽  
Renal Cortical Blood Flow ◽  
Renal Vascular ◽  
Inner Cortex ◽  
Equal Thickness ◽  
Total Renal Blood Flow

The involvement of prostaglandins in the redistribution of renal cortical blood flow to inner cortical nephrons during hemorrhagic hypotension was studied in the pentobarbital-anesthetized dog. Total renal blood flow and distribution of renal cortical flow were determined with the radioactive microsphere technique by dividing the cortex into four zones of equal thickness, zone 1 being outermost and zone 4 being juxtamedullary. Two inhibitors of prostaglandin synthesis were used: indomethacin 8 mg/kg and aspirin 100 mg/kg. The inhibitor or the vehicle was given intravenously prior to a control period which was followed by a hemorrhage sufficient to decrease arterial pressure by about one-third. The distribution of cortical flow was determined before hemorrhage, during hemorrhagic hypotension, and after transfusion. In the vehicle-treated dogs, total renal blood flow was well maintained, but flow redistributed to favor the inner cortical nephrons. This vasodilation in the inner cortex was blocked by both inhibitors of prostaglandin synthesis resulting in a decrease in total renal blood flow and relative ischemia of the juxtamedullary nephrons. Salicylate levels required to accomplish blockage of inner cortical vasodilaton were less than 7 mg/100 ml. These studies indicate that prostaglandins are responsible for the decreased vascular resistance of the inner cortical nephrons which results in the redistribution of blood flow during hemorrhage, and when prostaglandin synthesis is blocked, the kidney vasculature constricts during hemorrhage.

Influence of sodium intake on catecholamine release by angiotensin and renal nerve stimulation in dogs

1980 ◽  
Vol 58 (9) ◽  
pp. 1092-1101 ◽  
Author(s):  
Serge Carrière ◽  
Jean Cardinal ◽  
Christian Le Grimellec
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Sodium Intake ◽  
Regional Blood Flow ◽  
Blood Flow Rate ◽  
Renal Nerve ◽  
Salt Diet ◽  
Renal Nerve Stimulation ◽  
Total Renal Blood Flow

For 10 days, dogs were fed a normal salt diet containing 70 mequiv. Na+/day (NSD) followed by a high salt diet containing 170 mequiv. Na+/day (HSD) or 240 mequiv. Na+/day (VHSD), or the order was reversed. K+ in these diets was fixed at 40 mequiv./day. The different diets did not influence the basal level of serum catecholamines (CA). Intravenous angiotensin II (ATII) in subpressor doses produced, under NSD and HSD, an increase in serum CA accompanied by reductions in total renal blood flow as well as regional blood flow rates (microspheres), mostly in the deeper regions of the cortex. Under VHSD, ATII did not affect serum CA and barely decreased total renal blood flow, reducing regional blood flow rate in C3 and C4 only. The increase in renal vein serum CA produced by renal nerve stimulation was potentiated by ATII but under constant plasma levels of the latter, progressive increments of Na+ in the diet markedly exaggerated the liberation of CA following renal nerve stimulation and the hemodynamic response of the kidney. We conclude that the Na+ content in the diet markedly influences the increase in serum CA after renal nerve stimulation and greatly influences the response of that organ to renal nerve stimulation.

Influence of renal perfusion pressure on alpha- and beta-adrenergic stimulation of renin release

1985 ◽  
Vol 248 (3) ◽  
pp. E317-E326 ◽  
Author(s):  
M. L. Blair ◽  
Y. H. Chen ◽  
J. L. Izzo
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Neural Stimulation ◽  
Renin Release ◽  
Beta Blockade ◽  
Renal Perfusion Pressure ◽  
Stimulation Of ◽  
Total Renal Blood Flow

Experiments were performed in pentobarbital-anesthetized dogs to 1) determine if neural stimulation of renin release can be mediated by renal alpha-adrenoceptors at renal nerve stimulation (RNS) frequencies that have little or no effect on total renal blood flow (less than or equal to 1.2 Hz) and 2) ascertain whether alpha-adrenergic control of renin release is affected by renal perfusion pressure (RPP). The renal nerves were electrically stimulated both in the absence of RPP control and with RPP controlled near 85 mmHg. Decreased RPP lowered the threshold for neurogenic stimulation of renin release from less than or equal to 1.2 to 0.3 Hz. beta-Adrenoceptor blockade with propranolol blunted the renin secretion rate (RSR) response to graded RNS (0.3-5.0 Hz), but the extent of inhibition during low-frequency RNS was dependent on RPP. Propranolol prevented increased RSR at 0.6-1.2 Hz RNS when RPP was 111-120 mmHg but not when RPP was 85 mmHg. Combined alpha- and beta-blockade with prazosin and propranolol totally prevented increased RSR during 0.6-1.2 Hz RNS at reduced RPP. In summary, both alpha- and beta-adrenoceptors mediate neural stimulation of renin release at RNS frequencies that do not decrease total renal blood flow when RPP is 85 mmHg.

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