Influence of the plasma protein concentration on renal function

1991 ◽  
Vol 80 (5) ◽  
pp. 427-433 ◽  
Author(s):  
Allan D. Cumming ◽  
Adam Linton
Keyword(s):  
Renal Function ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Experimental Studies ◽  
Plasma Osmolality ◽  
Sodium Reabsorption ◽  
Plasma Protein Concentration

1. The effect of the plasma protein concentration on renal function remains controversial. Most, but not all, experimental studies suggest that a reduced plasma protein concentration perfusing the kidney may reduce tubular sodium reabsorption. Hypoproteinaemic disease states are usually associated with sodium retention, which is not always volume-dependent. 2. We induced a 21% and 24% reduction in plasma total protein and plasma albumin, respectively, in unanaesthetized sheep by acute extracorporeal plasmapheresis. Arterial pressure did not change, and changes in circulatory volume were minimised by infusion of crystalloid to maintain pulmonary artery occlusion pressure, measured using a Swann-Ganz pulmonary artery catheter. 3. After plasmapheresis, there was no significant change in creatinine clearance, sodium excretion, plasma renin activity or urinary kallikrein excretion. 4. After plasmapheresis, there was a significant reduction in plasma osmolality, increase in urine osmolality and fall in free water clearance. 5. The results suggest that in the absence of detectable changes in circulating volume or arterial pressure, acute hypoproteinaemia is associated with significant changes in renal water handling, but has no direct effect on sodium excretion or on renal release of renin and kallikrein.

Effect of arachidonic acid and indomethacin on renal function of dogs with pericardial tamponade

1981 ◽  
Vol 59 (6) ◽  
pp. 586-594 ◽  
Author(s):  
Robert J. Boudreau ◽  
Henry Mandin
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Pericardial Tamponade ◽  
Renin Activity ◽  
Plasma Protein Concentration

Previous studies revealed persistent sodium retention in dogs with chronic pericardial tamponade (induced by injection of Freund adjuvant into pericardial sacs) and pericardiocentesis, revealed in increased sodium excretion. Three groups of dogs were studied. Group 1 was treated with indomethacin (2.5 mg/kg, iv) prior to pericardiocentesis. Compared with experiments without indomethacin, sodium excretion did not increase following pericardiocentesis in animals treated with indomethacin despite similar changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity. This effect of indomethacin was presumably mediated through prostaglandin (PG) synthesis inhibition. Group 2 dogs received an infusion of arachidonic acid (AA) (to increase PG synthesis) into the left renal artery (20 μg∙kg−1∙min−1). Sodium excretion increased after AA infusion during tamponade (11.2 to 30.9 mequiv∙min−1) with a further increase occurring after pericardiocentesis (84.4 mequiv.∙min−1). Animals in group 3 were infused with both 20 and 80 μg∙kg−1∙min−1 doses of AA. Although sodium excretion following 80 μg∙kg−1∙min−1 AA (21 mequiv.∙min−1) was higher than that seen during 20 μg∙kg−1∙min−1 (14.2 mequiv.∙min−1), a further increase in sodium excretion to 45.6 mequiv.∙min−1 followed pericardiocentesis. During tamponade, AA did not change any of the measured parameters other than sodium excretion, a result compatible with the proposed distal tubular site of action of PG. Absolute but not fractional cortical blood flow distribution increased during the time sodium excretion increased following pericardiocentesis in all experiments. It is proposed that increased PG synthesis may be one possible mechanism involved in the natriuresis seen following pericardiocentesis. One cannot exclude the possibility that increased absolute blood flow to the superficial cortex also contributes to the observed natriuresis. Changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity appear to contribute to the observed natriuresis but only when PG synthesis is not blocked.

Effects of hypoproteinemia on blood volume and arterial pressure of volume-loaded dogs

1990 ◽  
Vol 259 (5) ◽  
pp. H1317-H1324
Author(s):  
R. D. Manning
Keyword(s):  
Body Weight ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Plasma Protein ◽  
Protein Concentration ◽  
Control Period ◽  
Plasma Protein Concentration ◽  
Autologous Plasma ◽  
Protein Mass

Studies were performed in 14 conscious, anephric dogs to clarify the role of blood volume in the genesis of hypertension. The dogs were splenectomized and had plasma protein concentration (PPC) reduced to 2.7 g/dl by daily plasmapheresis for 9 days. This hypoproteinemia resulted in a 20% decrease in both blood volume and mean arterial pressure. On the 10th day the dogs were nephrectomized. On the 11th day after a 3-h control period with plasmapheresis, lactated Ringer equivalent to 10 or 20% of body weight was intravenously infused. By 25 h postinfusion blood volume had not increased, and the dogs were still hypotensive. At 25 h plasma protein mass was returned to normal by intravenous infusion of autologous plasma, the average blood volume of the three low PPC groups increased approximately 50%, and the arterial pressure increased greater than 60%. The decrease in PPC shifted the regression of blood volume on sodium space down the blood volume axis. In conclusion, the dependence of arterial pressure on blood volume was demonstrated by the decrease in both blood volume and arterial pressure after PPC reduction, the constancy of blood volume and pressure during Ringer infusion, and the increase in both volume and pressure after plasma infusion.

Urinary kallikrein and systemic prostacyclin synthesis during sodium chloride infusion in normal man

1985 ◽  
Vol 68 (5) ◽  
pp. 537-543 ◽  
Author(s):  
M. L. Watson ◽  
A. D. Cumming ◽  
A. T. Lambie ◽  
J. A. Oates
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Urine Flow ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Plasma Protein Concentration

1. An intravenous infusion of 3 litres of sodium chloride solution (saline: 150 mmol/l) was given over 1 h to normal subjects. 2. During and immediately after the infusion, renal plasma flow increased in the majority of subjects, but the rise was not statistically significant. Significant increases in urine flow, sodium excretion, urinary kallikrein excretion and urinary excretion of dinor-6-keto prostaglandin (PG) F1α, a measure of systemic PGI2 synthesis, were noted. Plasma renin activity and plasma protein concentration were significantly lowered by the infusion. 3. At 2 h after the end of the infusion, although urine flow fell significantly, sodium excretion had not decreased. The reduction in plasma renin activity and plasma proteins persisted, and excretion of kallikrein and the PGI2 metabolite returned to control values. 4. Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. 5. The results suggest that increased systemic synthesis of PGI2 occurs in response to an acute infusion of sodium chloride, and may be an adaptive response of the vasculature to volume expansion. They support a role for the renal kallikrein-kinin system in the early diuretic and natriuretic response to saline infusion; the reduction in plasma renin activity and plasma protein concentration may be involved in both the early response and the persistent natriuresis 2 h after the infusion.

Effects of sustained lymph drainage on cardiovascular function and thoracic duct lymph in sheep

1989 ◽  
Vol 256 (4) ◽  
pp. R867-R874
Author(s):  
G. J. Valenzuela ◽  
C. W. Hewitt ◽  
G. C. Kramer ◽  
Y. Do ◽  
W. A. Hseuh
Keyword(s):  
Arterial Pressure ◽  
Plasma Protein ◽  
Thoracic Duct ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Escape Rate ◽  
Thoracic Duct Lymph ◽  
Lymph Drainage ◽  
Plasma Protein Concentration ◽  
Duct Lymph

We studied the effect of lowering the plasma protein concentration on the cardiovascular function and thoracic duct lymph in awake adult sheep. Hypoproteinemia was induced in seven nonpregnant, splenectomized sheep by drainage of the thoracic duct lymph over a 5-day period. The plasma protein went from a mean of 6.4 +/- 0.2 (SE) to 4.9 +/- 0.2 g/dl on day 5, and the lymph-to-plasma protein concentration ratio decreased from 0.74 +/- 0.01 on day 1 to 0.48 +/- 0.04 on day 5. The percentage composition of the protein fractions in plasma and lymph remained unchanged. Lymph flow was 1.79 +/- 0.37 and 1.28 +/- 0.10 ml/min for days 1 and 5, respectively. Renin concentration in plasma increased 50-fold by day 5. Arterial pressure fell from 102.9 +/- 5.4 to 72.7 +/- 4.4 mmHg by day 5. Mean hematocrit was 28.9 +/- 1.7 at day 1, which was not significantly different than 24.6 +/- 2.9 at day 5 and indicated that the plasma volume did not decrease. Body weight also did not change significantly. There was a decrease in the transcapillary protein escape rate, determined as the thoracic lymph flow rate multiplied the lymph protein concentration, that suggests adaptations in the microcirculation to decrease vascular-to-interstitial protein transfer during hypoproteinemia. Hypoproteinemic animals also demonstrated greater vascular retention of a fluid volume challenge. In conclusion, the sheep adaptations to sustained hypoproteinemia produced by lymph drainage were a significant decrease in arterial pressure, large increases in vascular compliance and renin concentration, and reduced transcapillary escape rate of protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of hypoproteinemia on fluid volumes and arterial pressure

1983 ◽  
Vol 245 (2) ◽  
pp. H284-H293 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Protein Concentration

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.

Renal hemodynamic, fluid volume, and arterial pressure changes during hyperproteinemia

1987 ◽  
Vol 252 (3) ◽  
pp. F403-F411 ◽  
Author(s):  
R. D. Manning
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Protein ◽  
Protein Concentration ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Plasma Protein Concentration

The chronic effects of hyperproteinemia on renal hemodynamics, fluid volume, and arterial pressure were determined in six conscious dogs over a 32-day period. Plasma protein concentration was increased by intravenous infusion of approximately 300 ml/day of previously collected autologous plasma, and the responses to changes in sodium intake were studied. By the end of a 9-day period of hyperproteinemia and normal sodium intake, plasma protein concentration had increased 2.2 g/dl, plasma colloid osmotic pressure had increased 7-8 mmHg, mean arterial pressure had increased 12 mmHg, glomerular filtration rate (GFR) had increased 15%, estimated renal plasma flow (ERPF) had increased 51% primarily due to renal vasodilatation, and filtration fraction had decreased 23%. Also, sodium balance was negative, water balance was positive, sodium iothalamate space had increased, plasma sodium concentration had decreased, and the relationship between mean arterial pressure and urinary sodium excretion was shifted to the right along the arterial pressure axis. In conclusion, long-term increases of plasma protein concentration result in a marked increase in ERPF as well as significant increases in GFR, extracellular fluid volume, and arterial pressure.

Effect of small-solute gradients on transcapillary fluid movement in renal inner medulla

1989 ◽  
Vol 257 (4) ◽  
pp. F547-F553 ◽  
Author(s):  
T. L. Pallone ◽  
Y. Yagil ◽  
R. L. Jamison
Keyword(s):  
Plasma Protein ◽  
Protein Concentration ◽  
Plasma Osmolality ◽  
Hydraulic Pressure ◽  
Osmotic Gradient ◽  
Plasma Protein Concentration ◽  
Fluid Movement ◽  
Vasa Recta ◽  
Renal Inner Medulla ◽  
Small Solute

Volume efflux from descending vasa recta (DVR) of hydropenic rats occurs despite a higher oncotic pressure than hydraulic pressure. To explain this, we previously proposed that transcapillary small-solute gradients exert an additional driving force for volume efflux. This hypothesis was tested by micropuncture of DVR at the base and tip of the exposed renal papilla of control hydropenic and furosemide-treated rats. The DVR plasma osmolality at the base, 573 +/- 40, rose to 1,011 +/- 118 mosmol/kg H2O at the tip in control animals but was 356 +/- 8 and 377 +/- 6, respectively in furosemide animals, demonstrating that the axial osmotic gradient was nearly eliminated. The DVR plasma protein concentration in control hydropenic rats was higher at the tip, 6.8 +/- 0.4 g/dl, than at the base, 5.2 g/dl (P less than 0.01), because of volume efflux from DVR between base and tip, but was 5.4 +/- 0.3 and 5.5 +/- 0.2 g/dl at the base and tip, respectively, in furosemide animals, indicating virtual abolition of volume efflux. In DVR at the tip in control animals, plasma protein concentration positively correlated with plasma osmolality (R = 0.72, P less than 0.02). These results support the hypothesis that transcapillary small-solute gradients influence transcapillary fluid movement in DVR.

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