Effect of hypophysectomy on sodium excretion in rats without blood dilution during blood volume expansion

1972 ◽  
Vol 28 (4) ◽  
pp. 471-472 ◽  
Author(s):  
B. Lichardus ◽  
J. Ponec
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Blood Volume Expansion ◽  
Blood Dilution

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.

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.

Renal nerves and renal responses to volume expansion in conscious monkeys

1988 ◽  
Vol 255 (3) ◽  
pp. R388-R394 ◽  
Author(s):  
T. V. Peterson ◽  
B. A. Benjamin ◽  
N. L. Hurst
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Denervation ◽  
Renal Excretion ◽  
Isotonic Saline ◽  
Urine Flow ◽  
Renal Nerves ◽  
Blood Volume Expansion ◽  
Renal Responses

Experiments were performed in conscious macaque monkeys to determine the effect of renal denervation on the diuresis and natriuresis of blood volume expansion. When the kidneys were innervated, expansion of estimated blood volume by 20% with 3% dextran in isotonic saline caused increases in urine flow (V), from 0.28 +/- 0.07 ml/min to a peak response of 1.08 +/- 0.20 ml/min, absolute sodium excretion (UNaV), from 30.0 +/- 11.2 to 99.8 +/- 11.7 mueq/min, and fractional sodium excretion (FENa+), from 1.24 +/- 0.51 to 3.19 +/- 0.56%. The animals then underwent bilateral renal denervation and were volume expanded a second time 6-13 days postdenervation. Under this condition, V increased from 0.32 +/- 0.05 to 0.64 +/- 0.08 ml/min, UNaV, from 22.2 +/- 4.6 to 46.2 +/- 8.0 mueq/min, and FENa+, from 0.91 +/- 0.26 to 1.92 +/- 0.41%, these increases being significantly less than when the kidneys were innervated. These results demonstrate that the renal nerves play an important role in the nonhuman primate in mediating increases in renal excretion during hypervolemia.

Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

1981 ◽  
Vol 241 (4) ◽  
pp. H571-H575 ◽  
Author(s):  
G. E. Billman ◽  
D. T. Dickey ◽  
K. K. Teoh ◽  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Position ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Baroreflex Control ◽  
Beta Receptor ◽  
Blood Volume Expansion ◽  
Beta Receptor Blockade

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

scholarly journals Gastroduodenal resistance and neural mechanisms involved in saline flow decrease elicited by acute blood volume expansion in anesthetized rats

1997 ◽  
Vol 30 (10) ◽  
pp. 1257-1256 ◽  
Author(s):  
J.R.V. Graça ◽  
F. de-A.A. Gondim ◽  
D.I.M. Cavalcante ◽  
J. Xavier-Neto ◽  
E.L.M. Messias ◽  
...  
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Neural Mechanisms ◽  
Anesthetized Rats ◽  
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.

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