Determinants of atrial natriuretic factor secretion in dogs expanded with isotonic saline or colloid solutions

1991 ◽  
Vol 69 (2) ◽  
pp. 145-153
Author(s):  
Peter Cernacek ◽  
Mortimer Levy
Keyword(s):  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Blood Volume ◽  
Bovine Serum ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Though increments in blood volume and atrial pressure are thought to be the primary stimuli for ANF secretion, plasma levels of this peptide do not always behave as a simple function of volume status. To outline the relationship between the latter and cardiac ANF release, we used five different volume-expansion protocols in anesthetized dogs. A stepwise expansion of plasma volume (PV) was achieved by two consecutive infusions: 0.9% saline followed or preceded by 4 or 25% bovine serum albumin (BSA), 4 or 25% dextran (Dx), or homologous plasma. Saline expansion led to a two- to four-fold increase in arterial plasma ANF level in all five protocols. Both 4 and 25% BSA caused no or very modest increase in plasma ANF, while all other colloid expanders caused the expected ANF release. In all protocols, plasma ANF closely correlated with central venous pressure (CVP). BSA expansion was the only protocol with no correlation between PV and ANF release. Changes in serum Ca2+ could not explain this finding. During BSA expansion, the lack of atrial response was related to the absence of increment (or even fall) in CVP despite the expanded PV. Similarly, urinary Na+ excretion was correlated both with CVP and ANF level but not with PV in BSA expansion. When the dogs were depleted of histamine before BSA infusion, the atrial secretory response was restored, suggesting that this colloid was associated with augmented capillary leakiness and vascular fluid efflux. These results show that the expansion of PV leads neither to ANF release nor to Na+ excretion if it is not accompanied by an expanded central blood volume with elevated atrial pressure.Key words: atrial natriuretic factor, volume expansion, isotonic saline, bovine serum albumin, dextran, homologous plasma.

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion

1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fetal Sheep ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of atrial natriuretic factor release by endothelin in ovine fetuses

1994 ◽  
Vol 267 (2) ◽  
pp. R380-R386 ◽  
Author(s):  
C. Y. Cheung
Keyword(s):  
Urinary Excretion ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Direct Action ◽  
Venous Pressure ◽  
Recovery Period ◽  
Control Period ◽  
Natriuretic Factor ◽  
Potent Vasoconstrictor ◽  
Atrial Natriuretic

Endothelin is a potent vasoconstrictor synthesized by vascular endothelial cells. In the adult, endothelin has been shown to stimulate the release of atrial natriuretic factor (ANF) through a direct action on atrial cardiocytes. The present study was designed to investigate, in the fetus, whether endothelin would similarly release ANF into the circulation. In addition, the effects of endothelin on fetal cardiovascular and urinary functions were explored. Chronically catheterized ovine fetuses between 126 and 139 days gestation (term 147 days) were used for the study. After a 30-min control period, the fetuses were infused intravenously with vehicle (n = 6) or endothelin-1 (n = 9) at 25 ng.min-1.kg-1 for 30 min, and this was followed by a 60-min recovery period. In response to endothelin infusion, plasma ANF levels were significantly elevated. Endothelin infusion acutely increased fetal arterial pressure without affecting venous pressure. Fetal heart rate decreased, and blood volume was reduced. Fetal urine flow rate and urinary excretion of electrolytes did not change during the endothelin infusion but were elevated during the recovery period. The fetus developed hypoxia and acidemia. Thus our study demonstrates that endothelin is effective in stimulating ANF release in the fetus, and this effect appears to be unrelated to the venous pressure changes. In addition, the results suggest that endothelin is a potent vasoconstrictor of the fetal systemic and umbilical vascular beds. The decrease in blood volume and increase in urinary excretion of fluid and electrolytes in response to endothelin are consistent with the known actions of ANF, which is elevated during endothelin infusion.

Release of atrial natriuretic factor in hypophysectomized rats

1988 ◽  
Vol 255 (4) ◽  
pp. R534-R538 ◽  
Author(s):  
J. R. Dietz ◽  
S. J. Nazian
Keyword(s):  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Isolated Heart ◽  
Endocrine Function ◽  
Intact Group ◽  
Natriuretic Factor ◽  
Blood Volume Expansion ◽  
Intact Rats ◽  
Atrial Natriuretic

The purpose of these studies was to examine the effect of hypophysectomy (HYPOX) on the secretion of atrial natriuretic factor (ANF) and related changes in renal function. Pentobarbital sodium-anesthetized rats received a 20% intravenous blood volume expansion. In intact rats (n = 7), plasma ANF was 39 +/- 3 pg/ml before volume expansion and increased to 71 +/- 10 and 77 +/- 7 pg/ml after volume expansion (P less than 0.01). Volume expansion in HYPOX rats (n = 8) also resulted in an increase in plasma ANF concentration that was significantly less than in the intact group. With volume expansion, sodium excretion rate increased from 0.19 +/- 0.06 to 1.43 +/- 0.43 microM. min-1.100 g body wt-1 (P less than 0.01) in intact rats and from 0.24 +/- 0.08 to 0.74 +/- 0.14 microM.min-1.100 g body wt-1 (P less than 0.05) in HYPOX rats (HYPOX less than intact; P less than 0.05). In an isolated heart-lung preparation, HYPOX rats secreted significantly less ANF than intact rats during two 30-min perfusion periods (P less than 0.02). Atrial ANF concentration was also significantly less in HYPOX rats (P less than 0.05). These results show that hypophysectomy leads to an attenuation of the ANF response to atrial distention and attenuated natriuretic response to blood volume expansion and suggest that the pituitary is required to maintain normal cardiac endocrine function.

Plasma vasopressin and atrial natriuretic factor in response to blood volume changes in the anaesthetized rabbit

1989 ◽  
Vol 67 (4) ◽  
pp. 344-352 ◽  
Author(s):  
C. A. Courneya ◽  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Vagal Afferents ◽  
Right Atrial ◽  
Volume Changes ◽  
Natriuretic Factor ◽  
Vagal Afferent ◽  
Aortic Baroreceptors ◽  
Atrial Natriuretic

The influence of aortic baroreceptors and vagal afferent nerves on the release of immunoreactive vasopressin (iVP) and immunoreactive atrial natriuretic factor (iANF) was examined in anaesthetized rabbits. Changes in plasma concentrations of iVP and iANF, heart rate, mean arterial pressure, and right atrial pressure were measured in response to blood volume changes (+20, +10, −10, −20%). Carotid sinus pressure was maintained at 100 mmHg (1 mmHg = 133.3 Pa), and blood volume changes were performed before and after bilateral vagotomy (VNX) in all experiments. Two experimental groups were studied: rabbits with aortic depressor nerves intact (ADNI) and those with aortic depressor nerves sectioned (ADNX). Mean arterial and right atrial pressures decreased during haemorrhage and increased in response to volume expansion. Plasma iVP concentrations increased with haemorrhage and decreased with volume expansion in the ADNI group. Plasma iANF, however, decreased with haemorrhage and increased during volume expansion in both ADNI and ADNX groups. Vagotomy caused an increase in baseline plasma iANF in the ADNX group. The responses of iANF to blood volume changes were augmented after VNX and ADNX. The results show that neither the aortic baroreceptor nor the vagal afferent input are needed for the iANF response to changes in blood volume, over the range of ± 20%. In contrast, intact aortic baroreceptors are essential for changes in circulating iVP in this preparation.Key words: vasopressin, atrial natriuretic factor, blood volume, aortic baroreceptors, vagal afferents.

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.

Cardiovascular and fluid responses to atrial natriuretic factor in sheep fetus

1987 ◽  
Vol 253 (4) ◽  
pp. R561-R567 ◽  
Author(s):  
R. A. Brace ◽  
C. Y. Cheung
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Flow Rate ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Presently little is known about the effects of atrial natriuretic factor (ANF) in the fetus. In this study we explored the effects of ANF on vascular pressures and fluid dynamics in the chronically catheterized sheep fetuses averaging 133 days gestation (term = 145-150 days). Under resting conditions plasma ANF concentration was positively correlated with fetal heart rate (P less than 0.001) and was not correlated with arterial pressure, venous pressure, or plasma osmolality. The weight-normalized fetal urine flow rate correlated positively with ANF concentration (P less than 0.01). After a bolus injection of 8 micrograms/kg of synthetic human ANF into the inferior vena cava, fetal arterial pressure decreased by 2 mmHg and remained at this level for 60 min, venous pressure was unchanged, and heart rate increased transiently by 15 beats/min. Urine flow rate increased to 250% of control 5 min after the injection and returned to control at 20 min even though ANF was four times control levels. Fetal blood volume decreased significantly by 5% within 10 min and remained low for 60 min. This decrease in blood volume was greater than the increase in urine flow. A kinetic analysis revealed that ANF disappearance from the plasma could not be adequately characterized with a single rate constant due to exchange between plasma and interstitial fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

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