Hypoproteinemia and recovery from edema in dogs

1988 ◽  
Vol 254 (6) ◽  
pp. F887-F894
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
W. Kortlandt ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Plasma Protein ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Recovery Period ◽  
Plasma Renin ◽  
Colloid Osmotic Pressure ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Sodium Balance ◽  
Low Protein

We studied the effects of hypoproteinemia following 12 days of repeated plasmapheresis and low-protein diet on sodium balance, fluid volumes, and renal hemodynamics in six conscious dogs on 50 mmol sodium intake. Measurements during hypoproteinemia were obtained during a 5-day recovery period starting 20 h after the final plasmapheresis session, with continued low-protein diet. During the plasmapheresis period sodium was retained. Sodium balance became negative on the first recovery day when plasma protein was 29 +/- 1 g/l (control 60 +/- 2 g/l, P less than 0.01), and plasma colloid osmotic pressure (COP) was 9 +/- 1 mmHg (control 22 +/- 1 mmHg, P less than 0.01). Subcutaneous fluid COP was lowered from 14 +/- 1 to 4 +/- 1 mmHg (P less than 0.01). Blood volume, plasma renin activity, and aldosterone were unchanged. Glomerular filtration rate and effective renal plasma flow were slightly reduced (NS), and filtration fraction was unchanged. After a second plasmapheresis period in three of the dogs, plasma protein fell to 26 +/- 1 g/l and COP to 7 +/- 1 mmHg. Now sodium was retained on the first day after stopping plasmapheresis, and renin and aldosterone were high. The next day, when plasma protein was again 29 +/- 1 g/l and COP 8 +/- 1 mmHg, these three dogs were able to completely excrete an infusion of 130 mmol sodium. These data suggest that the level of plasma COP below which dogs on a medium-sodium intake would retain sodium averages 8 mmHg, which is considerably lower than generally thought.

Increased NaCl preference of rats fed low-protein diet

1996 ◽  
Vol 270 (6) ◽  
pp. R1189-R1196 ◽  
Author(s):  
A. Okiyama ◽  
K. Torii ◽  
M. G. Tordoff
Keyword(s):  
Control Diet ◽  
Physiological Mechanism ◽  
Plasma Renin ◽  
Calcium Deficiency ◽  
Protein Deficiency ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Sodium Balance ◽  
Deficient Diet ◽  
Low Protein

Four studies were conducted to assess the effect of a low-protein diet on NaCl intake. Young rats fed either control (20% casein) or low-protein (5% casein) high-carbohydrate (CHO) diet were allowed to drink either water alone or water and 300 mM NaCl. Relative to rats fed control diet, rats fed the low-protein diet progressively increased NaCl intake so that, despite lower food and water intakes, they drank 180% more NaCl during the last 3 days of the 21-day test. Additional studies found that rats fed low-protein diet always maintained positive sodium balance, were neither sodium depleted nor hypovolemic, and had normal plasma renin activity and aldosterone concentrations. The elevated NaCl intake was not secondary to calcium deficiency and was unaffected by mineral supplementation of the protein-deficient diet. Increases in the diet's CH and/or fat content incidental to decreases in its protein content influenced, but could not completely account for, the effect of protein deficiency on NaCl intake. We conclude that protein deficiency is the primary cause of the elevated NaCl preference produced by being fed a low-protein diet and that a novel physiological mechanism underlies this behavior.

scholarly journals Biochemical observations on rat aorta: interaction of dietary protein and cholesterol

1986 ◽  
Vol 55 (2) ◽  
pp. 295-304 ◽  
Author(s):  
S. P. Bydlowski ◽  
V. L. G. Stivaletti ◽  
C. R. Douglas
Keyword(s):  
Total Cholesterol ◽  
Plasma Protein ◽  
Recovery Period ◽  
Diet Group ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Temporary Increase ◽  
Cholesterol Feeding ◽  
Low Protein ◽  
Standard Protein

1. The effect of cholesterol feeding during and after a period of protein malnutrition lasting 4 weeks was examined in the rat. Indices measured were plasma total cholesterol, triglycerides and protein levels, and aorta total cholesterol, triglycerides, hexosamine and hydroxyproline concentrations.2. In both plasma and aorta, total cholesterol and triglycerides levels were higher in the low-protein diet group than in the standard-protein diet group, when cholesterol was supplied in both diets.3. During the malnutrition period, cholesterol feeding led to a greater decrease in plasma protein than that promoted by the low-protein diet without cholesterol, while aorta hexosamine levels decreased to a lesser extent.4. Cholesterol feeding with a standard-protein diet promoted a slight and temporary increase in aorta hydroxyproline levels, while a decrease in aorta hexosamine concentration was observed. Cholesterol feeding with the low-protein diet, on the other hand, also promoted a decrease in aorta hexosamine levels but to a lesser extent.5. During the recovery period, cholesterol feeding impaired the return of plasma protein, aorta hexosamine and lipid levels to that of the control values.6. These findings demonstrate that cholesterol feeding promotes different changes in aorta and plasma, depending on whether or not protein is supplied by the diet in adequate amounts. This point could be important in relation to the development of atherosclerosis during recovery from a period of malnutrition.

scholarly journals Plasma proteins in growing analbuminaemic rats fed on a diet of low-protein content

1989 ◽  
Vol 61 (3) ◽  
pp. 485-494 ◽  
Author(s):  
J. A. Joles ◽  
E. H. J. M. Jansen ◽  
C. A. Laan ◽  
N. Willekes-Koolschijn ◽  
W. Kortlandt ◽  
...  
Keyword(s):  
Body Weight ◽  
Osmotic Pressure ◽  
Plasma Protein ◽  
Protein Concentration ◽  
Extracellular Fluid ◽  
Colloid Osmotic Pressure ◽  
Protein Diet ◽  
Sprague Dawley ◽  
Plasma Protein Concentration ◽  
Low Protein

1. Analbuminaemic and Sprague-Dawley (control) rats were fed on low- (60 g/kg) protein and control (200 g protein/kg) dietsad lib.from weaning. Males and females were studied separately. Body-weight and plasma protein concentrations were determined at 10 d intervals from 25 to 75 d of age. Electrophoresis of plasma proteins was performed in samples from day 75. Extracellular fluid volume was measured at 10 d intervals from day 45 onwards. Colloid osmotic pressure was measured in plasma and interstitial fluid (wick technique) at the start and end of the trial.2. Body-weight increased much less on the low-protein diet than on the normal diet in both strains and sexes. The growth retardation was slightly more pronounced in the male analbuminaemic rats than in the male Sprague-Dawley controls.3. Plasma protein concentration increased during normal growth in all groups, particularly in the female analbuminaemic rats. This increase was reduced by the 60 g protein/kg diet in all groups, with the exception of the male analbuminaemic rats.4. Differences in plasma colloid osmotic pressure were similar to those seen in plasma protein concentration. Interstitial colloid osmotic pressure was higher in the control rats than in the analbuminaemic ones. The interstitial colloid osmotic pressure increased during growth in the control but not in the analbuminaemic rats. The difference in interstitial colloid osmotic pressure between the strains was maintained during low-protein intake, but at a lower level than during normal protein intake.5. Subtracting interstitial from plasma colloid osmotic pressure, resulted in a rather similar transcapillary oncotic gradient in the various groups at 75 d, both on the control protein diet (11–14 mmHg), and on the lowprotein diet (9–11 mmHg).6. All protein fractions were reduced to a similar extent by the low-protein diet in the control rats, whereas in the analbuminaemic rats protein fractions produced in the liver were more severely depressed.7. Extracellular fluid volume as a percentage of body-weight was similar in all groups, and decreased with increasing age.8. In conclusion, the analbuminaemic rats were able to maintain the transcapillary oncotic gradient on both diets by reducing the interstitial colloid osmotic pressure. Oedema was not observed.9. Despite the absence of albumin, the protein-malnourished analbuminaemic rat is no more susceptible to hypoproteinaemia and oedema than its normal counterpart.

Weanling Rats Exposed to Maternal Low-Protein Diets during Discrete Periods of Gestation Exhibit Differing Severity of Hypertension

1996 ◽  
Vol 91 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Simon C. Langley-Evans ◽  
Simon J. M. Welham ◽  
Rachel C. Sherman ◽  
Alan A. Jackson
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Plasma Renin ◽  
Late Gestation ◽  
Protein Diet ◽  
Male Rats ◽  
Low Protein Diet ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat, hypertension is induced by fetal exposure to maternal low-protein diets. The effect on blood pressure of undernutrition before conception and during discrete periods in early, mid or late pregnancy was assessed using an 18% casein (control) diet and a 9% casein diet to apply mild protein restriction. 2. The offspring of rats fed 9% casein developed raised blood pressure by weaning age. Feeding a low-protein diet before conception was not a prerequisite for programming of hypertension. 3. Hypertension was observed in rats exposed to low protein during the following gestational periods: days 0–7, days 8–14 and days 15–22. Blood pressure increases elicited by these discrete periods of undernutrition were lower than those induced by feeding a low-protein diet throughout pregnancy. The effect in early gestation was significant only in male animals. Post-natal growth of male rats exposed to low-protein diets was accelerated, but kidneys were small in relation to body weight. 4. Biochemical indices of glucocorticoid action in liver, hippocampus, hypothalamus and lung were elevated in rats exposed to low-protein diets in utero. The apparent hypersensitivity to glucocorticoids was primarily associated with undernutrition in mid to late gestation. 5. Plasma renin activity was elevated in rats exposed to 9% casein over days 15–22 of gestation. Animals undernourished over days 0–7 and 8–14 produced pups with lower plasma angiotensin II concentrations at weaning. 6. Fetal exposure to maternal low-protein diets for any period in gestation may programme hypertension in the rat. Alterations to renal structure, renal hormone action or the hypothalamic—pituitary-adrenal axis may all play a role in the programming phenomenon, either independently or in concert.

Protein intake regulates the vasodilatory function of the kidney and NMDA receptor expression

2004 ◽  
Vol 287 (5) ◽  
pp. R1184-R1189 ◽  
Author(s):  
Larry A. Slomowitz ◽  
Francis B. Gabbai ◽  
Ser J. Khang ◽  
Joseph Satriano ◽  
Sonia Thareau ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Protein Intake ◽  
Renal Plasma Flow ◽  
Receptor Expression ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Western Blots ◽  
Low Protein ◽  
Protein Feeding

Glycine infusion in normal rats causes an increase in renal plasma flow and glomerular filtration rate (GFR). Although the renal response to glycine infusion is well characterized, the mechanism initiating this vasodilation is unknown. We recently observed functionally active N-methyl-d-aspartate (NMDA) receptors in the kidney, located primarily in tubular structures. The mechanisms regulating activity of the NMDA receptor within the kidney are also unknown, as is its normal day-to-day functional role. Therefore, we hypothesize that dietary protein may impact the functional response to glycine infusion in both untreated rats and rats pretreated with angiotensin-converting enzyme (ACE) inhibitor and, furthermore, that renal NMDA receptors may be involved in the glycine response. Surprisingly, 2 wk of low-protein diet (8% protein vs. 21% protein in control diet) totally inhibited the glycine-induced vasodilation and GFR response. Associated with the absence of renal vasodilation, a significant reduction in proximal tubular reabsorption was observed during glycine infusion in low-protein-diet rats. In contrast to the disease models previously studied in our laboratory, administration of ACE inhibitors did not restore the glycine response in rats treated with low-protein diet. Western blots of normal- and low-protein-diet kidneys demonstrate that the newly described renal NMDA receptor is downregulated in rats fed a low-protein diet. Low-protein feeding results in loss of glycine-induced vasodilation and GFR responses associated with decreased renal NMDA receptor expression. Kidney NMDA receptor expression is conditioned by protein intake, and this receptor may play an important role in the kidney vasodilatory response to glycine infusion and protein feeding in rats.

Effect of amino acid infusion on renal hemodynamics in humans

1986 ◽  
Vol 251 (1) ◽  
pp. F132-F140 ◽  
Author(s):  
P. Castellino ◽  
B. Coda ◽  
R. A. DeFronzo
Keyword(s):  
Amino Acid ◽  
Protein Intake ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Base Line ◽  
Acid Infusion ◽  
Amino Acid Infusion ◽  
Low Protein

The effect of amino acid (AA) infusion on renal hemodynamics was examined in 19 healthy subjects. Thirteen subjects participated in the first protocol (normal protein intake) and six in the second protocol (low protein intake). The first protocol consisted of three studies: study 1 (n = 13), AA were infused over 3 h to increase plasma amino acid levels two- to threefold; study 2 (n = 7), AA were infused with somatostatin and peripheral replacement of insulin, glucagon, and growth hormone; study 3 (n = 6), somatostatin was infused with basal hormonal replacement as in study 2. During study 1, glomerular filtration rate (GFR) rose by 20% (from 107 +/- 5 to 128 +/- 4 ml . 1.73 m-2 . min-1, P less than 0.001). Renal plasma flow (RPF) increased by a similar percentage (599 +/- 35 to 704 +/- 33 ml . 1.73 m-2 . min-1, P less than 0.001). When somatostatin was infused with AA (study 2), neither GFR nor RPF changed from base line. Somatostatin infusion alone (study 3) had no effect on GFR or RPF. During protocol 2, six subjects received a low-protein diet (40 g/day) for 7 days and AA were infused as per study 1. Base-line GFR (104 +/- 5 to 96 +/- 4 ml . 1.73 m-2 . min-1 and RPF (593 +/- 32 to 507 +/- 23 ml . 1.73 m-2 . min-1) both decreased (P less than 0.02) after the low-protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Pathogenesis of oedema in protein-energy malnutrition: the significance of plasma colloid osmotic pressure

1979 ◽  
Vol 42 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Marta Fiorotto ◽  
W. A. Coward
Keyword(s):  
Interstitial Fluid ◽  
Control Diet ◽  
Protein Energy Malnutrition ◽  
Colloid Osmotic Pressure ◽  
Protein Diet ◽  
Water Filtration ◽  
Low Protein Diet ◽  
Oedema Formation ◽  
Low Protein ◽  
Protein Energy

1. Rats were made oedematous by feeding them low-protein diets (protein: energy (P:E) 0.005) ad lib., and measurements were made of plasma and interstitial fluid colloid osmotic pressures (πp and πi respectively) and interstitial fluid hydrostatic pressure (Pi) before, and at the onset of, oedema formation. Taken together as (πp − πi + Pi) these forces oppose capillary pressure (Pc) and thus determine rates of transcapillary water filtration. Interstitial fluid was sampled, in non-oedematous and oedematous animals, from perforated capsules implanted subcutaneously for the measurement of Pi. Blood, plasma and interstitial fluid volumes were also determined.2. In Expt I comparisons were made between animals fed on a control diet (P:E 0.210) and the lowprotein diet. In normal animals the ratio πp:πi was approximately 2, but in protein deficiency it was increased since reductions in the absolute value of πi matched those in πp. These changes were observed 2 weeks after the start of the experiment and became more exaggerated when oedema appeared (weeks 18–22).3. Pi was normally negative with respect to atmospheric pressure but increased to values close to zero when oedema formation occurred.4. Despite the reductions in πp that were seen in the protein-deficient animals the sum of the forces opposing filtration (πp − πi + Pi) did not change significantly during the experiment.5. Plasma and interstitial fluid volumes expressed per kg body-weight (measured using 125I-albumin and 35SO42−) were unchanged as πp initially decreased in the protein-deficient animals but increased markedly with the onset of oedema.6. In Expt 2 comparisons were made between animals fed the low-protein diet ad lib. and others fed on the control diet in restricted amounts so that weight loss was the same in the two groups of animals.7. The wasting induced by restriction of the control diet did not produce reductions in πp or πi and values for Pi were normal. Changes in the animals fed on the low-protein diet were similar to those observed in Expt I. By using 51Cr-labelled erythrocytes it was shown that the expansion in plasma volume that occurred when oedema appeared in the protein-deficient animals was mainly due to a reduction in total erythrocyte volume. Blood volume did not increase significantly.8. It was concluded that in the hypoproteinaemia induced in the experimental animals reductions in the value of πp, which might otherwise result in an imbalance of forces that would produce excessive rates of transcapillary water filtration, were compensated for by reductions in πi. Increases in Pi also compensated but were quantitatively less important.9. The significance of the results is discussed in terms of the pathogenesis of oedema in kwashiorkor and the concept of an oncotic threshold for oedema formation in hypoproteinaemia.

Evidence that intrarenal bradykinin plays a role in regulation of renal function

1993 ◽  
Vol 265 (4) ◽  
pp. E648-E654 ◽  
Author(s):  
H. M. Siragy
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Kinin System ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

Bradykinin (BK) is produced by the kidney, but the role of the renal kallikrein-kinin system (KKS) in the control of renal function is not understood. We studied the effects of intrarenal infusion of the BK antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid (BKA, n = 5) and BK (n = 4) alone or combined with antagonist (BKA 0.025 ng.kg-1 x min-1 + BK 0.25 ng.kg-1 x min-1, n = 4) in uninephrectomized conscious dogs in sodium balance at 10 and 80 meq/day. During low sodium intake, administration of BKA (infusions from 0.025 to 2.5 ng.kg-1 x min-1) caused a significant antidiuresis (P < 0.0001) and antinatriuresis (P < 0.0001) and a decrease in fractional sodium excretion (P < 0.0001). There were no changes in estimated renal plasma flow (RPF) or glomerular filtration rate during intrarenal administration of BKA at 0.025 and 0.25 ng.kg-1 x min-1. A dose of 2.5 ng.kg-1 x min-1 BKA caused a significant decrease in RPF. There were no changes in plasma aldosterone concentration, plasma renin activity, or systemic arterial pressure during intrarenal BKA administration. At 80 meq/day sodium balance (n = 5), intrarenal administration of BKA did not cause any systemic or renal effects. Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Coinfusion of BK with BKA completely abrogated the renal excretory changes induced by BKA. These data suggest that intrarenal KKS plays a role in control of renal function largely by a tubular mechanism during low sodium intake.

Glomerular and hormonal responses to dietary protein intake in human renal disease

1987 ◽  
Vol 253 (6) ◽  
pp. F1083-F1090 ◽  
Author(s):  
M. E. Rosenberg ◽  
J. E. Swanson ◽  
B. L. Thomas ◽  
T. H. Hostetter
Keyword(s):  
Dietary Protein ◽  
High Protein Diet ◽  
Plasma Renin ◽  
High Protein ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Prostaglandin E ◽  
Glomerular Diseases ◽  
Low Protein ◽  
Fractional Clearance

The effects of dietary protein on glomerular and hormonal function were studied in twelve adults with a variety of glomerular diseases. They were randomly assigned, using a crossover design, to two 11-day periods, one on a high-protein diet (2 g.kg-1.day-1) and the other on a low-protein diet (0.55 g.kg-1.day-1). Improvement in glomerular permselectivity on the low-protein diet was manifested by a decreased 24-h urinary excretion of total protein, albumin, and IgG by 33, 40, and 25%, respectively (all P less than 0.02); a fall in the fractional clearance of albumin (10.1 +/- 6.3 X 10(-3) to 5.8 +/- 3.3 X 10(-3)), and IgG (6.9 +/- 5.1 X 10(-3) to 3.5 +/- 2.3 X 10(-3)) (both P less than 0.02); and a decreased fractional clearance of neutral dextrans of molecular radii 48-56 A (P less than 0.05), when measured on the final day of each dietary period. The high-protein diet was accompanied by a higher plasma renin activity (6.9 +/- 1.6 vs. 3.5 +/- 0.8 ng angiotensin I.ml-1.h-1) (P less than 0.02), and increased excretion of prostaglandin E and 6-ketoprostaglandin F1 alpha. We conclude that a low-protein diet rapidly improves the size-selective defect in glomerular permselectivity.

scholarly journals BLOOD PLASMA PROTEIN REGENERATION AS INFLUENCED BY FASTING, INFECTION, AND DIET FACTORS

1938 ◽  
Vol 67 (5) ◽  
pp. 675-690 ◽  
Author(s):  
S. C. Madden ◽  
W. E. George ◽  
G. S. Waraich ◽  
H. Whipple
Keyword(s):  
Blood Plasma ◽  
Plasma Protein ◽  
Building Material ◽  
Protein Production ◽  
Basal Diet ◽  
The Body ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Body Protein ◽  
Low Protein

When blood plasma proteins are depleted by bleeding, with return of the washed red cells (plasmapheresis) it is possible to bring dogs to a steady state of hypoproteinemia and a uniform plasma protein production on a basal low protein diet. These dogs are clinically normal with normal appetite, no anemia and normal nitrogen metabolism. These dogs become test subjects by which various factors relating to plasma protein production may be tested. The normal dog (10 to 13 kg.) has a substantial reserve store of plasma protein building material (10 to 60+ gm.) which requires 2 to 6 weeks plasmapheresis for its complete removal. After this period the dog will produce uniform amounts of plasma protein each week on a fixed basal diet. Dogs previously depleted by plasmapheresis and then permitted to return to normal during a long rest period of many weeks, may show much higher reserve stores of protein building material in subsequent periods of plasma depletion (see Table 1). Under uniform conditions of low protein diet intake when plasmapheresis is discontinued for 2 weeks the plasma protein building material is stored quantitatively in the body and can subsequently be recovered (Table 4) in the next 2 to 3 weeks of plasmapheresis. Given complete depletion of plasma protein building reserve stores the dog can produce very little (2± gm. per week) plasma protein on a protein-free diet. This may be related to the wear and tear of body protein and conservation of these split products. Abscesses produced in a depleted dog during a fast may cause some excess production of plasma protein which is probably related to products of tissue destruction conserved for protein anabolism. Gelatin alone added to the basal diet causes very little plasma protein production but when supplemented by tryptophane gives a large protein output, while tryptophane alone is inert.

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