Effect of Blood Volume Expansion on Basal Plasma Atrial Natriuretic Factor and Adrenocorticotropic Hormone Secretions in the Fetal Rat at Term

Neonatology ◽  
1994 ◽  
Vol 65 (6) ◽  
pp. 390-395 ◽  
Author(s):  
S. Deloof ◽  
A. Chatelain
Keyword(s):  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Adrenocorticotropic Hormone ◽  
Natriuretic Factor ◽  
Blood Volume Expansion ◽  
Fetal Rat ◽  
Basal Plasma ◽  
Hormone Secretions ◽  
Atrial Natriuretic

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.

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.

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.

The contribution of atrial natriuretic factor to acute volume natriuresis in rats

1987 ◽  
Vol 253 (6) ◽  
pp. F1129-F1135 ◽  
Author(s):  
R. W. Barbee ◽  
N. C. Trippodo
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Urinary Sodium Excretion ◽  
Right Atrial ◽  
Natriuretic Factor ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

To explore the role of atrial natriuretic factor (ANF) in acute volume-expansion natriuresis, right atrial pressure (RAP), mean arterial pressure (MAP), rate of urinary sodium excretion (UNaV), and plasma immunoreactive ANF (IR-ANF) were measured in anesthetized, open-chest rats. All groups received 33% blood volume expansion with whole blood in 15 min. RAP was not allowed to increase in one group by using a caval snare. MAP was controlled in a second group with the use of an aortic snare. A third group (RAP-controlled ANF) with control of RAP received rat ANF (99-126) at doses designed to mimic the IR-ANF measured in the MAP-controlled rats. IR-ANF was similar 5 min after blood infusion in rats exhibiting increased RAP (490 +/- 111 pg/ml) and in those without increased RAP but receiving ANF infusion (447 +/- 44 pg/ml); this was also true at 45 min after blood infusion (232 +/- 44 vs. 263 +/- 27 pg/ml). IR-ANF in rats with constant RAP (without ANF infusion) remained low throughout the experiment (61 +/- 10 and 74 +/- 10 pg/ml). UNaV increased only in the MAP-controlled and ANF-infused groups, but peak responses occurred 15-30 min after the onset of volume expansion in the former, and 60-75 min in the latter. Thus, factors other than ANF mostly accounted for the immediate natriuresis after volume expansion, whereas ANF predominated after a delayed period. The results suggest that increased plasma ANF accounted for at least 34% of the observed natriuretic response to acute volume expansion in anesthetized rats.

Relationship between atrial granularity and release of atrial natriuretic factor in rats with diabetes mellitus

1989 ◽  
Vol 257 (4) ◽  
pp. R932-R938 ◽  
Author(s):  
R. A. Hebden ◽  
M. E. Todd ◽  
J. H. McNeill
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Pressure Control ◽  
Diabetic Rats ◽  
Right Atrial ◽  
Morphological Examination ◽  
Natriuretic Factor ◽  
Blood Volume Expansion ◽  
Right Atria ◽  
Atrial Natriuretic

We examined the effect of a 25% blood volume expansion on the release of atrial natriuretic factor (ANF) in conscious Wistar rats (13-15 wk old) injected 6 wk earlier with streptozotocin (55 mg/kg iv, diabetic) or saline (1 ml/kg iv, control). The diabetic rats demonstrated a significant (P less than 0.05) resting hypotension (132 +/- 2/91 +/- 1 mmHg, systolic/diastolic) and bradycardia (340 +/- 5 beats/min) compared with the controls (145 +/- 2/98 +/- 2 mmHg, 377 +/- 8 beats/min). Resting plasma immunoreactive (IR) ANF levels were significantly (P less than 0.05) elevated in the diabetic rats (control: 72 +/- 4 pg/ml; diabetic: 87 +/- 4), although resting right atrial pressures were not different (control: 6.0 +/- 0.8 cmH2O; diabetic: 5.2 +/- 0.6). Volume expansion with donor blood from similarly treated animals significantly (P less than 0.05) elevated IR ANF levels in both groups, but the increase in the saline-injected group (+527 +/- 80 pg/ml) was significantly (P less than 0.05) greater than that of the streptozotocin-injected group (+323 +/- 45 pg/ml). Both groups showed similar elevations in right atrial pressure (control: +1.8 +/- 0.3 cmH2O; diabetic: +1.6 +/- 0.4). Morphological examination of tissue taken from right atria demonstrated no difference in cardiocyte volume percent per unit of tissue but a significant (P less than 0.05) reduction in the relative frequency of occurrence of atrial granules in the diabetic group. The cause of the reduction in atrial granularity in these animals is as yet unknown.

Neural influences on renal responses to acute volume expansion in rats with heart failure

1996 ◽  
Vol 271 (4) ◽  
pp. H1441-H1448 ◽  
Author(s):  
K. P. Patel ◽  
P. L. Zhang ◽  
P. K. Carmines
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerve ◽  
Natriuretic Factor ◽  
Renal Nerve Activity ◽  
Neural Influences ◽  
Renal Responses ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

Experiments were performed to test the postulate that neural influences underlie the suppressed excretory response to acute volume expansion (VE) typically observed 3-4 wk after myocardial infarction to induce chronic heart failure (CHF). Responses to VE were assessed in innervated (intact) and denervated (DNX) kidneys of anesthetized CHF rats and sham-operated controls. CHF rats exhibited blunted natriuretic responses to VE in both intact kidneys (35% of sham response) and DNX kidneys (55% of sham DNX response). CHF rats also displayed suppressed excretory responses to atrial natriuretic factor (0.25 microgram.kg-1.min-1 iv) in both intact kidneys (74% of sham response) and DNX kidneys (63% of sham DNX response). Additional experiments confirmed that the compliance of the venoatrial junction did not differ between sham rats (52 +/- 2 mmHg/microliter) and CHF rats (54-2 mmHg/microliter). The observations support the contention that both tonic renal sympathetic renal nerve activity and suppressed renal atrial natriuretic factor responsiveness likely contribute to the blunted excretory response to VE during CHF.

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