Water and Sodium Excretion after Blood Volume Expansion under Conditions of Constant Arterial, Venous and Plasma Oncotic Pressures and Constant Haematocrit

1972 ◽  
Vol 42 (6) ◽  
pp. 701-709 ◽  
Author(s):  
B. Lichardus ◽  
A. Nizet
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Specific Factor ◽  
Experimental Conditions ◽  
Natriuretic Hormone ◽  
Arterial Perfusion ◽  
Homologous Blood Transfusion ◽  
Blood Volume Expansion

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.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

Chronic atrial appendectomy alters sodium excretion in conscious monkeys

1988 ◽  
Vol 254 (4) ◽  
pp. R699-R705
Author(s):  
B. A. Benjamin ◽  
C. H. Metzler ◽  
T. V. Peterson
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Sham Group ◽  
Venous Pressure ◽  
Urine Flow ◽  
Central Venous ◽  
Renal Response ◽  
Fractional Sodium Excretion ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

The purpose of this study is to determine whether chronic removal of atrial appendages alters renal response to volume expansion in the conscious monkey. Chronic bilateral atrial appendectomy (ATX) was performed in six animals. Six additional animals served as sham-operated controls. Monkeys were studied 1-2 wk after chronic surgery. The protocol consisted of three consecutive 10-min urine collections followed by 20% ischemic blood volume expansion (VE) and 120 min of post-VE measurements. In sham animals, VE caused an increase in plasma atrial natriuretic peptide (ANP) levels (48 +/- 7 pg/ml to a peak of 108 +/- 34 pg/ml). Urine flow increased from 0.43 +/- 0.07 to 1.07 +/- 0.24 ml/min, sodium excretion increased from 17.9 +/- 2.6 to 74.9 +/- 12.0 mu eq/min, and fractional sodium excretion increased from 0.67 +/- 0.10 to 2.43 +/- 0.28%. ATX attenuated the increase in ANP (34 +/- 8 pg/ml to a peak of 38 +/- 9 pg/ml) in four of six animals. In these animals, renal response to VE was significantly attenuated. Urine flow increased from 0.21 +/- 0.05 to 0.30 +/- 0.01 ml/min, sodium excretion increased from 19.3 +/- 6.02 to 37.8 +/- 5.05 mu eq/min, and fractional sodium excretion increased from 0.79 +/- 0.08 to 1.43 +/- 0.17%. Renal response of two ATX animals with normal increases in atrial natriuretic factor was similar to the sham group. Effect of volume expansion on mean arterial pressure, central venous pressure, and renal hemodynamics was not altered by ATX. These findings demonstrate that bilateral atrial appendectomy in the monkey attenuates the increase in ANP and reduces renal response to VE.

Baroreflex regulation of hindquarter vascular resistance during acute blood volume expansion

1984 ◽  
Vol 246 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
G. B. Guo ◽  
D. R. Richardson
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Time Course ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Baroreflex Control ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors ◽  
Cardiopulmonary Baroreceptors

The baroreflex control of hindquarter vascular resistance in response to a 30% blood volume expansion (BVE) was examined in constant-flow perfused hindlimbs of chloralose-urethan-anesthetized rats. Volume expansion initially increased both systemic arterial pressure (SAP) and central venous pressure (CVP) while decreasing hindquarter vascular resistance. After these initial changes, there was a parallel return of hindquarter-vascular resistance and CVP to pre-expansion levels, suggesting that cardiopulmonary afferents play a major role in the vascular resistance adjustments to volume expansion. This notion was supported in a separate set of experiments in which CVP was elevated selectively while SAP was held constant. This manipulation elicited a decrease in hindquarter vascular resistance, which was significantly attenuated following vagal cardiopulmonary denervation. The return of hindquarter vascular resistance following BVE also occurred in the presence of elevated SAP in rats with vagotomy and aortic nerve denervation, i.e., only the carotid sinus baroreflexes intact, but the time course was much faster compared with preparations with cardiopulmonary receptors intact. No response of hindquarter vascular resistance to BVE was observed in rats with both sinoaortic and cardiopulmonary baroreceptors denervated. These findings suggest that the return of hindquarter vascular resistance following BVE involves a gradual increase in sympathetic outflow to the hindquarters resulting from both a decrease in cardiopulmonary afferent activity and a rapid adaptation of arterial baroreflexes.

Rat venular pressure-diameter relationships are regulated by sympathetic activity

1990 ◽  
Vol 259 (3) ◽  
pp. H674-H680 ◽  
Author(s):  
A. A. Shoukas ◽  
H. G. Bohlen
Keyword(s):  
Blood Volume ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Nervous System Activity ◽  
Blood Volume Expansion ◽  
Capacitance Characteristics ◽  
Sympathetic Nervous ◽  
Relationship Of ◽  
The Relationship

The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.

ANF secretion and renal responses to volume expansion with equilibrated blood

1988 ◽  
Vol 255 (5) ◽  
pp. F936-F943 ◽  
Author(s):  
R. V. Paul ◽  
T. Ferguson ◽  
L. G. Navar
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
High Dose ◽  
Sprague Dawley ◽  
Blood Volume Expansion ◽  
Step Procedure ◽  
Sprague Dawley Rats ◽  
Fractional Excretion Of Sodium

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.

Natriuretic peptide receptor A mediates renal sodium excretory responses to blood volume expansion

2003 ◽  
Vol 285 (4) ◽  
pp. F694-F702 ◽  
Author(s):  
Shang-Jin Shi ◽  
Elangovan Vellaichamy ◽  
So Yeon Chin ◽  
Oliver Smithies ◽  
L. Gabriel Navar ◽  
...  
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Urinary Flow ◽  
Natriuretic Peptide Receptor ◽  
Wild Type ◽  
Peptide Receptor ◽  
Blood Volume Expansion ◽  
Natriuretic Peptide Receptor A

The deficiency of Npr1 [genetic determinant of natriuretic peptide receptor A (NPRA)] increases arterial pressures and causes hypertensive heart disease in mice similar to those seen in untreated human hypertensive patients. However, the quantitative role of NPRA in mediating the renal responses to blood volume expansion remains uncertain. To determine the specific contribution of NPRA in mediating the signaling mechanisms responsible for natriuretic and diuretic responses to nondilutional intravascular expansion, we administered whole blood to anesthetized Npr1 homozygous null mutant (0-copy), wild-type (2-copy), and gene-duplicated (4-copy) mice. In wild-type (2-copy) animals, urinary flow (μl · min–1 · g kidney wt–1) increased from 4.9 ± 1.0 to 14.4 ± 1.8 and sodium excretion (μeq · min–1 · g kidney wt–1) from 1.15 ± 0.22 to 3.11 ± 0.60, associated with a rise in glomerular filtration rate (GFR; ml · min–1 · g kidney wt–1) from 0.63 ± 0.03 to 0.82 ± 0.09 and renal plasma flow (RPF; ml · min–1 · g kidney wt–1) from 2.96 ± 0.17 to 4.36 ± 0.41, whereas arterial pressure did not significantly increase. After volume expansion, 0-copy mice showed significantly lesser increases in urinary flow ( P < 0.001) and sodium excretory ( P < 0.001) responses even though the increases in arterial pressures were greater ( P < 0.001) compared with 2-copy mice. The 4-copy mice showed augmented responses in urinary flow ( P < 0.01) and sodium excretion ( P < 0.001) along with rises in both GFR ( P < 0.01) and RPF ( P < 0.01) compared with 2-copy wild-type mice. These results establish that NPRA activation is the predominant mechanism mediating the natriuretic, diuretic, and renal hemodynamic responses to acute blood volume expansion.

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
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Whole Blood ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Filtration Fraction ◽  
Natriuretic Hormone ◽  
Blood Volume Expansion ◽  
Measured Volume

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.

Lack of Effect of Blood-Volume Expansion on Short-Circuit Current across an Isolated Toad Skin Incorporated in the Circulation of a Rat

1978 ◽  
Vol 55 (1) ◽  
pp. 15-21
Author(s):  
D. Querido ◽  
L. C. Isaacson
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Systemic Blood Pressure ◽  
Ringer Solution ◽  
Detectable Effect ◽  
Toad Skin ◽  
Natriuretic Hormone ◽  
Blood Volume Expansion

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.

Increased ANF secretion after volume expansion is preserved in rats with heart failure

1988 ◽  
Vol 254 (2) ◽  
pp. R185-R191 ◽  
Author(s):  
Y. W. Chien ◽  
R. W. Barbee ◽  
A. A. MacPhee ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Blood Volume ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Blood Volume Expansion

To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P less than 0.01), cardiac index (-27%, P less than 0.001), renal blood flow (-35%, P less than 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P less than 0.01), and increases in central venous pressure (+1.7 mmHg, P less than 0.01), left ventricular end-diastolic pressure (+10 mmHg, P less than 0.001), total peripheral resistance (+28%, P less than 0.01), and plasma ANF level (752 +/- 109 vs. 244 +/- 33 pg/ml, P less than 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricle pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 +/- 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.

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