Blood-Volume Expansion in the Rat: Natriuresis Accompanied by a Fall in Filtration Fraction

1981 ◽  
Vol 60 (3) ◽  
pp. 283-293
Author(s):  
D. Querido ◽  
L. C. Isaacson

1. We have attempted to confirm the existence of a natriuretic hormone released in response to acute expansion of blood volume. 2. Isolated kidneys, perfused with whole blood at constant pressure, were incorporated within an extracorporeal circulation in recipient rats. In six control experiments urine flow rate, renal blood flow, glomerular filtration rate, filtration fraction, and the fractional excretion of filtered sodium and water were measured for periods of up to 120–140 min thereafter. The same variables were measured in a further 12 experiments in which, after 63 ± 11 min, the rats were volume expanded with equilibrated whole blood (15, 18 or 28 ml/kg body wt.). 3. On average the controls revealed no change in any of the variables measured; volume expansion was followed by increased renal blood flow and fractional excretion of filtered sodium and water, while the filtration fraction fell. 4. In both the control and volume-expansion experiments, there were 12 instances in which the fractional excretion of filtered sodium increased; in 10 of these, including those experiments in which the natriuresis was most marked, there was a closely correlated fall in filtration fraction. 5. In all the experiments changes in the fractional excretion of filtered sodium and water varied in parallel. 6. We conclude that volume expansion (a) changes the concentration of some circulating vasoactive substance(s) and (b) results in natriuresis and diuresis consequent upon a fall in filtration fraction.

1988 ◽  
Vol 255 (5) ◽  
pp. F936-F943 ◽  
Author(s):  
R. V. Paul ◽  
T. Ferguson ◽  
L. G. Navar

To evaluate the role of atrial natriuretic factor (ANF) in the renal response to acute blood volume expansion without hemodilution, a reservoir syringe filled with donor rat blood was connected to the femoral artery and vein of anesthetized Sprague-Dawley rats to allow rapid equilibration of the reservoir with the intravascular blood. Volume expansion with blood from the reservoir in two steps (of 1 and 1.5% body wt, separated by 1 h, n = 5 rats) produced a mean peak increase in plasma immunoreactive ANF from 99 +/- 21 to 1,310 +/- 230 pg/ml (P less than 0.001); plasma ANF levels throughout these experiments correlated significantly with simultaneously measured urine flow (r = 0.74, P less than 0.005) and sodium excretion (r = 0.65, P less than 0.005). Another group (n = 7) underwent the same two-step procedure; after the second volume expansion, high-dose atriopeptin III infusion (0.4 microgram.kg-1.min-1 did not further increase fractional excretion of sodium (3.17 +/- 0.27 to 2.50 + 0.39%, P = NS). In another group (n = 9 rats), the same dose of atriopeptin III was started before any blood volume expansion. After the resulting hypotension was corrected by restoration of blood volume, an additional 1.5% body weight blood volume expansion did not further augment sodium excretion. We conclude that the diuresis and natriuresis, which occur in response to volume expansion without hemodilution, rise and fall in parallel with immunoreactive ANF in the plasma, and that ANF and acute blood volume expansion act on the kidney through a similar, saturable mechanism.


1978 ◽  
Vol 55 (1) ◽  
pp. 15-21
Author(s):  
D. Querido ◽  
L. C. Isaacson

1. Evidence for the existence of ‘natriuretic hormone’ resides, in part, in the demonstration that blood volume expansion in the dog is followed by a transient fall in short-circuit current (SCC) across a frog skin incorporated within its circulation. 2. We have attempted to confirm this effect in the rat, with a toad skin (Xenopus laevis) incorporated within the circulation. The skins, bathed in whole rat blood, displayed low SCC; skins bathed in ‘mammalian’ Ringer solution displayed equally low SCC, but responded normally to pitressin or amiloride. 3. When volume expansion was induced in ten rats by infusion of equilibrated whole blood (28 ml/kg body weight) there was a brisk rise in systemic blood pressure, diuresis, natriuresis and kaliuresis. 4. This blood-volume expansion was without detectable effect on the SCC across the skins incorporated within the rats' circulations.


1972 ◽  
Vol 42 (6) ◽  
pp. 701-709 ◽  
Author(s):  
B. Lichardus ◽  
A. Nizet

1. The diuretic and natriuretic responses occurring during expansion of blood volume by homologous blood transfusion were studied in homologous kidneys transplanted to the neck of hydropenic dogs that had previously been given deoxycorticosterone acetate and antidiuretic hormone. The experimental conditions ensured constant arterial perfusion pressure, venous pressure, osmotic pressure, haematocrit and plasma oncotic pressure. 2. Moderate but significant increases in urine output, renal sodium excretion, osmotic clearance and tubular sodium rejection fraction were observed; there were no significant changes in glomerular filtration rate, renal blood flow, postglomerular haematocrit and postglomerular plasma protein concentration 20 and 40 min after the end of blood infusion. 3. As the non-hormonal factors known to modulate sodium excretion underwent no significant change, the results are compatible with the proposition that a specific factor (‘natriuretic hormone’) plays a role in the mechanism of natriuresis after blood volume expansion.


Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3603-3610 ◽  
Author(s):  
Amy G. Tsai ◽  
Pedro Cabrales ◽  
Belur N. Manjula ◽  
Seetharama A. Acharya ◽  
Robert M. Winslow ◽  
...  

Abstract Cell-free hemoglobin's (CFH) high affinity for nitric oxide (NO) could limit CFH's use as an oxygen-carrying blood replacement fluid because it scavenges NO, causing vasoconstriction and hypertension. However, the extent to which perivascular NO levels change following intravascular administration of hemoglobin (Hb) with different molecular dimensions correlates with vasoconstrictive responses in the microcirculation is unknown. The study objective was to determine vasoconstrictive effects following bolus infusions of (1) αα cross-linked Hb; (2) polymerized bovine Hb; or (3) polyethylene glycol-decorated Hb (PEG-Hb), by measurements of in vivo microvessel diameter, blood flow, perivascular NO concentration, and systemic hemodynamic parameters. All CFHs caused reductions in perivascular NO levels, not correlated to microvascular responses. PEG-Hb (largest molecular volume) maintained blood flow, while the others caused vasoconstriction and reduced perfusion. All solutions increased mean arterial pressure due to vasoconstriction and blood volume expansion, except for PEG-Hb, which increased blood pressure due to blood volume expansion and maintenance of cardiac output. In conclusion, perivascular NO reduction is similar for all Hb solutions because NO binding affinities are similar; however, effects on vascular resistance are related to the type of molecular modification, molecular volume, and oxygen affinity.


1977 ◽  
Vol 52 (4) ◽  
pp. 351-356
Author(s):  
G. J. Kaloyanides ◽  
Loren Cohen ◽  
G. F. DiBona

1. Selected organ-ablation experiments were performed in dogs in an attempt to identify the source of the natriuretic hormone postulated to participate in the natriuresis of blood volume expansion. 2. An isolated dog kidney perfused with blood from the femoral artery of deoxycorticosterone-loaded dogs subjected to acute volume expansion with equilibrated blood served as the bioassay system for the natriuretic factor. Four groups were studied after the following procedures: group I, no ablation; group II, thyroparathyroidectomy; group III, hypophysectomy; group IV, adrenalectomy. 3. In all groups, the administration of equilibrated blood promoted a significant increase in sodium chloride excretion in the isolated kidney. The natriuresis was unrelated to changes in glomerular filtration rate, renal blood flow, renal arterial pressure, plasma protein concentration or packed cell volume. In the absence of volume expansion, sodium chloride excretion in the isolated kidney did not change or decreased. 4. These results argue against the thyroid, parathyroid, adrenal and pituitary glands as the source of natriuretic hormone.


1972 ◽  
Vol 50 (5) ◽  
pp. 463-466 ◽  
Author(s):  
A. T. Veress ◽  
J. W. Pearce

Bilateral cervical vagotomy in the rat reduces the diuretic but not the natriuretic response to vascular expansion by infusion of whole blood. The attenuation of volume diuresis is similar to that observed in rats with intact vagus nerves but receiving an infusion of pitressin as well as the vascular expansion. The findings are consistent with the Gauer–Henry reflex, which attributes volume diuresis in part to reflex inhibition of vasopressin release, but imply that vagal afferents are not involved in volume natriuresis.


1990 ◽  
Vol 22 (2) ◽  
pp. S102
Author(s):  
K. Norton ◽  
M. Delp ◽  
M. Jonas ◽  
C. Duan ◽  
D. Dengel ◽  
...  

1990 ◽  
Vol 69 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
M. T. Jones ◽  
C. Duan ◽  
D. R. Dengel ◽  
...  

To study the distribution of blood flow after blood volume expansion, seven miniature swine ran at high speed (17.6-20 km/h, estimated to require 115% of maximal O2 uptake) on a motor-driven treadmill on two occasions: once during normovolemia and once after an acute 15% blood volume expansion (homologous whole blood). O2 uptake, cardiac output, heart rate, mean arterial pressure, and distribution of blood flow (with radiolabeled microspheres) were measured at the same time during each of the exercise bouts. Maximal heart rate was identical between conditions (mean 266); mean arterial pressure was elevated during the hypovolemic exercise (149 +/- 5 vs. 137 +/- 6 mmHg). Although cardiac output was higher and arterial O2 saturation was maintained during the hypervolemic condition (10.5 +/- 0.7 vs. 9.3 +/- 0.6 l/min), O2 uptake was not different (1.74 +/- 0.08 vs. 1.74 +/- 0.09 l/min). Mean blood flows to cardiac (+12.9%), locomotory (+9.8%), and respiratory (+7.5%) muscles were all elevated during hypervolemic exercise, while visceral and brain blood flows were unchanged. Calculated resistances to flow in skeletal and cardiac muscle were not different between conditions. Under the experimental conditions of this study, O2 uptake in the miniature swine was limited at the level of the muscles during hypervolemic exercise. The results also indicate that neither intrinsic contractile properties of the heart nor coronary blood flow limits myocardial performance during normovolemic exercise, because both the pumping capacity of the heart and the coronary blood flow were elevated in the hypervolemic condition.


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