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.

Renal response to volume expansion in atrial-appendectomized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. R786-R793
Author(s):  
B. A. Benjamin ◽  
C. H. Metzler ◽  
T. V. Peterson
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Control Period ◽  
Urine Flow ◽  
Central Venous ◽  
Renal Response ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

The purpose of this study was to determine whether chronic removal of the atrial appendages alters the renal response to volume expansion (VE) in anesthetized dogs. Chronic bilateral atrial appendectomy (ATX) was performed in 10 animals. Six animals served as sham-operated controls (S). The animals were studied 10-14 days after chronic surgery. The protocol consisted of a 20-min control period followed by isochemic VE (20%) and 120 min of post-VE measurements. The dogs were studied a second time, 2 wk later, after acute bilateral cervical vagotomy. Results from the vagi-intact study showed that VE caused a diuresis, natriuresis, and increase in fractional sodium excretion in ATX that did not differ from the response observed in S. VE also caused equivalent increases in central venous and mean arterial pressures in S and ATX. Atrial appendectomy, however, failed to significantly attenuate the increase in atrial natriuretic factor (ANF) after VE. Plasma ANF increased from 27.2 +/- 4.8 to 47.0 +/- 7.3 pg/ml in ATX and from 27.2 +/- 7.8 to 59.0 +/- 17.9 pg/ml in S. After vagotomy, VE caused transient increases in urine flow and sodium excretion. The changes in central venous and mean arterial pressures were not different from the vagi-intact study and vagotomy did not affect the increase in ANF after VE. Circulating ANF levels increased from 26.4 +/- 5.5 to 75.0 +/- 14.0 pg/ml in ATX and from 28.1 +/- 5.7 to 73.0 +/- 22.6 pg/ml in S. These results demonstrate that, in the dog, bilateral ATX does not alter the renal response to volume expansion or attenuate the increase in ANF. In addition, these results show that vagal pathways are not required for the release of ANF and that vagotomy fails to uncover any effect of atrial appendectomy on renal function.

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.

The Role of Cardiopulmonary Sympathetic Afferents in Blood Volume Homoeostasis in the Non-Human Primate

1983 ◽  
Vol 64 (3) ◽  
pp. 281-287 ◽  
Author(s):  
Kurtis G. Cornish ◽  
Joseph P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Free Water ◽  
Urine Flow ◽  
Central Venous ◽  
Free Water Clearance ◽  
Human Primate

1. Four Macaca fascicularis monkeys were bilaterally sympathectomized by removing the thoracic sympathetic chain from the middle cervical ganglion to the T-6 sympathetic ganglion. This was done chronically, allowing adequate recovery time. While under light pentobarbital anaesthesia, the animals were then subjected to blood volume expansions with isotonic, isooncotic dextran or to head-out immersions. Seven immersions and seven volume expansions were carried out. 2. With immersion, there were significant increases in blood pressure, central venous pressure, urine flow, sodium excretion, potassium excretion, glomerular filtration rate, percentage of filtered sodium excreted and free water clearance. Although blood pressure and central venous pressure initially increased during the first immersion period, heart rate continued to increase with the immersion, while blood pressure and central venous pressure remained constant. Volume expansion caused an increase in central venous pressure, urine flow, sodium and potassium excretion, osmolar clearance, free water clearance, percentage of filtered sodium excreted and glomerular filtration rate. 3. Since these results with both the immersions and volume expansions were not qualitatively different from those observed in control animals, it is concluded that cardiopulmonary sympathetic afferents are not necessary for the renal response to head-out immersion or blood volume expansion in the non-human primate.

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.

Plasma release of atrial natriuretic peptide in response to blood volume expansion

1986 ◽  
Vol 109 (1) ◽  
pp. 9-13 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Christofides ◽  
S. R. Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Colloidal Solution ◽  
Venous Pressure ◽  
Molecular Size ◽  
Rat Plasma ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

ABSTRACT The response of plasma atrial natriuretic peptide (ANP) concentration to acute intravascular volume expansion was measured in ten male Wistar rats. An infusion of 3 ml polygelene colloidal solution at 37 °C over 45 s produced peak venous pressure rises of 1·5cm water. A highly significant (P<0·001) rise of immunoreactive plasma ANP from 24·4 ± 2·2 (mean ± s.e.m.) pmol/l to a peak of 70·0±10·5 pmol/l occurred within 2·5 min. Plasma ANP concentrations had virtually returned to basal levels (32·7 ± 2·7 pmol/l) 30 min after this acute volume load. A further infusion of 10 ml polygelene colloidal solution in 2 min produced peak venous pressure rises of 10 cm water and caused a dramatic and significant (P< 0·001) increase of plasma ANP concentration to a peak of 534·8 ± 38·5 pmol/l, occurring 7·5 min after infusion. The plasma ANP concentration had fallen but remained above basal levels 30 min later (137·2 ± 26·4 pmol/l). Similar results were obtained using an identical protocol but with whole rat blood instead of polygelene solution as the volume-expanding agent. Gel column chromatography suggested that the majority of the immunoreactive ANP in rat plasma was of similar molecular size to rat α-ANP(1–28). These results support the hypothesis that blood volume expansion is a potent stimulus for the release of ANP into plasma. J. Endocr. (1986) 109, 9–13

Influence of volume expansion on hemodynamic effects of atrial natriuretic factor in rabbits

1989 ◽  
Vol 256 (3) ◽  
pp. H852-H858
Author(s):  
M. Volpe ◽  
A. Cuocolo ◽  
F. Vecchione ◽  
G. Lembo ◽  
S. Pignalosa ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Constant Infusion ◽  
Hemodynamic Effects ◽  
Central Venous ◽  
Natriuretic Factor ◽  
Induced Changes ◽  
Renal Responses ◽  
Atrial Natriuretic

We investigated the influence of acute volume expansion on the hemodynamic and renal responses to the constant infusion of atrial natriuretic factor (ANF) (alpha-human ANP, 2 micrograms/kg bolus, 0.2 microgram.kg-1.min-1) in rabbits anesthetized with ketamine and acepromazine. The effects of the peptide were evaluated in 12 euvolemic rabbits and in 15 rabbits during the steady-state phase of volume expansion (0.9% NaCl 4.5 ml/min for 60 min). In the euvolemic animals, ANF caused an increase in natriuresis and a reduction in blood pressure (BP), which was associated with a decrease in cardiac output (CO), stroke volume (SV), and no significant changes in central venous pressure (CVP), peripheral hematocrit (Hct), and heart rate (HR). When the peptide was infused in the volume-expanded animals, the effects of ANF on BP and HR were comparable with those observed in the euvolemic animals. However, in these animals the ANF-induced changes in CO, SV, CVP, and Hct were significantly greater than those observed in the euvolemic group. In addition, the percent increases in diuresis and natriuresis were significantly smaller than those obtained in the euvolemic animals. In conclusion, volume expansion with saline potentiates the effects of ANF on systemic hemodynamics and blood volume.

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.

Role of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion

1993 ◽  
Vol 129 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Kazutoshi Sato ◽  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Hypertonic Saline ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Central Venous ◽  
Plasma Volume Expansion ◽  
Natriuretic Hormone ◽  
Atrial Natriuretic Hormone ◽  
Atrial Natriuretic

To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCI alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined. Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D-HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.

Cardiac output and renal excretion rates during acute blood volume expansion in rats

1978 ◽  
Vol 234 (1) ◽  
pp. H21-H27 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Volume Expansion ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Plasma Protein Concentration ◽  
Renal Response ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

Selected central vascular parameters and renal excretion rates were monitored in anesthetized rats after acute, isohemic blood volume expansion by 33 percent. The infusate was an equilibrated mixture of animals' own blood and isotonic, isoncotic (6 percent) bovine albumin. Expansion increased mean arterial pressure by 35 percent, mean central venous pressure (CVP) by 850 percent, cardiac output (CO) by 56 percent, hematocrit (Hct) by 25 percent, plasma protein concentration (Ppr) by 25 percent, renal excretion rates of volume by 4,400 percent, of sodium by 2,800 percent, and of potassium by 360 percent of the respective preinfusion value. Hct and Ppr measurements suggested that 15 min after the end of the infusion, only 33 percent of infused volume remained within the circulation and that there was little further change in this during the remainder of the experiment. At the end of the elevated renal response, CVP and CO alone had returned to control values. Renal excretion rates were highly correlated with CO, but they were delayed by 2-5 min with respect to it. The results suggest that the renal response to acute volume expansion does not primarily control blood volume. Cardiac output may be the controlled variable in the response.

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