Chronic vs. acute hemodynamic effects of atrial natriuretic factor in conscious rats

1991 ◽  
Vol 260 (1) ◽  
pp. R247-R254 ◽  
Author(s):  
L. M. Harrison-Bernard ◽  
R. C. Vari ◽  
W. H. Holleman ◽  
N. C. Trippodo ◽  
R. W. Barbee
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Hemodynamic Effects ◽  
Vascular Volume ◽  
Control Value ◽  
Natriuretic Factor ◽  
Chronic Infusion ◽  
Atrial Natriuretic

The present study was designed to examine acute (2 h) and chronic (5 day) effects of pathophysiological elevations of plasma atrial natriuretic factor (ANF) in conscious normotensive rats. Acute infusion of ANF (100 ng.kg-1.min-1; n = 15) resulted in a decrease in mean arterial pressure (MAP) of 5 +/- 3 mmHg, which was associated with a 23 +/- 4% decrease in cardiac output (CO) and a 27 +/- 6% increase in total peripheral resistance (TPR). Hematocrit increased from 41.9 +/- 0.7 to 46.0 +/- 0.6%, which is suggestive of vascular volume contraction. Chronic infusion of ANF (n = 9) produced a significant fall in MAP from a control value of 114 +/- 2 to 100 +/- 3 and 99 +/- 2 mmHg on days 1 and 5, respectively. CO decreased significantly (27 +/- 2%) and TPR increased (21 +/- 5%) on day 1; neither variable was significantly different from control on day 5. Plasma immunoreactive ANF levels were significantly elevated during acute (791 +/- 76 pg/ml) and chronic (626 +/- 202 pg/ml) ANF infusion compared with control values of approximately 100 pg/ml. The results indicate that elevations in plasma ANF within the pathophysiological range can significantly alter systemic hemodynamics, initially mediated by a decrease in CO. Autoregulatory phenomena may counteract these hemodynamic effects, returning CO to control levels and reducing TPR when the elevations in plasma ANF are chronically sustained.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

Differing hemodynamic responses to atrial natriuretic factor in two models of hypertension

1986 ◽  
Vol 250 (5) ◽  
pp. H871-H878 ◽  
Author(s):  
M. Volpe ◽  
R. E. Sosa ◽  
F. B. Muller ◽  
M. J. Camargo ◽  
N. Glorioso ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Hemodynamic Parameters ◽  
Hypertensive Rats ◽  
Hemodynamic Responses ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Hemodynamic responses to synthetic atrial natriuretic factor (ANF), were studied in renin-dependent two-kidney, one-clip (2K,1C) and deoxycorticosterone (DOC) salt-treated hypertensive rats as well as normotensive controls. ANF infusion (800 pmol/kg prime, 120 pmol X kg-1 X min-1 for 60 min) decreased blood pressure (BP) more in conscious 2K,1C (-24 +/- 4%) than in DOC salt-treated (-12 +/- 4%, P less than 0.05) or control rats. Hemodynamic parameters were also evaluated during graded infusion of three doses, each for 30 min. At 24 and 120 pmol X kg-1 X min-1, ANF lowered BP in 2K,1C rats, both conscious (from 156 +/- 6 to 144 +/- 7, P less than 0.05 and 135 +/- 5 mmHg, P less than 0.05) and anesthetized (from 148 +/- 7 to 138 +/- 7, P less than 0.05 and 128 +/- 7, P less than 0.05). In anesthetized 2K,1C, BP changes were associated with reduction in total peripheral resistance (TPR) that became significant at 120 pmol X kg-1 X min-1 (-10 +/- 2%), whereas cardiac output (CO) and stroke volume (SV) were unchanged. In DOC-salt-treated rats these doses did not lower BP despite progressive falls in CO (-7 +/- 3% and -24 +/- 5%, P less than 0.05) and SV (-8 +/- 2% and -23 +/- 5%, P less than 0.05), which were balanced by a simultaneous rise in TPR (+12 +/- 4% and +26 +/- 10%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of clonidine and dihydralazine on atrial natriuretic factor and cGMP in humans

1989 ◽  
Vol 67 (3) ◽  
pp. 938-944 ◽  
Author(s):  
M. Wehling ◽  
T. Muller ◽  
J. M. Heim ◽  
R. Lorenz ◽  
H. Witzgall ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Soluble Guanylate Cyclase ◽  
Normal Subjects ◽  
Treated Group ◽  
Base Line ◽  
Hemodynamic Effects ◽  
Volume Loading ◽  
Natriuretic Factor ◽  
Basal Plasma ◽  
Atrial Natriuretic

The effects of a 1-wk treatment with clonidine (75 micrograms/day twice a day) and dihydralazine (25 mg/day twice a day) on base-line levels of plasma atrial natriuretic factor (ANF) and plasma and urinary guanosine 3′,5′-cyclic monophosphate (cGMP) and their changes by acute saline infusion (2 liters) in eight normal subjects were evaluated. Basal ANF was decreased to 65% in the clonidine group compared with both the control and dihydralazine groups. Volume loading increased plasma ANF levels by 30–40% of base-line values in the control and the dihydralazine groups and by 15% in the clonidine group. Basal plasma and urinary cGMP levels were raised by 30 and 90% in the dihydralazine group compared with both other groups. Volume loading increased plasma cGMP levels by 40% in the control and clonidine-treated groups and by 25% in the dihydralazine-treated group. It is concluded that ANF may contribute to hemodynamic effects of clonidine but not to those of dihydralazine. Dihydralazine increases plasma and urinary cGMP, supposedly by direct activation of the soluble guanylate cyclase.

Responses of vasoactive hormones in congestive cardiac failure

1987 ◽  
Vol 65 (8) ◽  
pp. 1706-1711 ◽  
Author(s):  
C. I. Johnston ◽  
L. F. Arnolda ◽  
K. Tsunoda ◽  
P. A. Phillips ◽  
G. P. Hodsman
Keyword(s):  
Heart Failure ◽  
Cardiac Failure ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Congestive Cardiac Failure ◽  
Renin Angiotensin ◽  
Natriuretic Factor ◽  
Vasoactive Hormones ◽  
Atrial Natriuretic

Congestive cardiac failure causes activation of various neurohumoral responses that increase total peripheral resistance and promote salt and water retention. These effects increase blood pressure and organ perfusion in the short term, but ultimately cause further cardiac decompensation by increasing ventricular afterload and cardiac work. The role of the renin–angiotensin–aldosterone system and the catecholamines is partially understood, and blockade of these systems as a treatment of heart failure is now established. The role of vasopressin in heart failure is more controversial, but there is now compelling evidence that vasopressin may have important vasoconstrictor actions in addition to its fluid retaining properties. Atrial natriuretic factor is a newly described cardiac hormone released from the atrium. Atrial natriuretic factor causes natriuresis, diuresis, vasodilatation, suppression of thirst, and suppression of both renin and aldosterone. These actions largely counteract the effects of the renin–angiotensin system and vasopressin. Plasma atrial natriuretic factor has been reported to be markedly elevated in human and experimental heart failure, and may act to limit the neurohumoral response to reduced cardiac output. This review summarizes our understanding of the vasoactive hormones and reports experimental evidence supporting a pathophysiological role for vasopressin and atrial natriuretic factor in congestive cardiac failure.

Immunoreactive atrial natriuretic factor is increased in ovine model of endotoxemia

1988 ◽  
Vol 254 (4) ◽  
pp. R567-R571
Author(s):  
H. J. Lubbesmeyer ◽  
L. Woodson ◽  
L. D. Traber ◽  
J. T. Flynn ◽  
D. N. Herndon ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Causative Factor ◽  
Capillary Absorption ◽  
Ovine Model ◽  
Hemodynamic Changes ◽  
Potential Mediator ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

A bolus of Escherichia coli endotoxin (1.5 micrograms/kg) was administered to chronically instrumented sheep. Immunoreactive atrial natriuretic factor (IR-ANF) was measured in extracted plasma by radioimmunoassay. There was a thirteenfold increase in IR-ANF 2 h after endotoxin administration, and IR-ANF levels remained significantly elevated during the first 6 h. A marked diuresis and natriuresis occurred between 4 and 6 h. ANF not only affects renal function but is also associated with decreased cardiac output, increased peripheral resistance (in sheep), and decreased capillary absorption (in rats). These renal and hemodynamic changes are also characteristic of the early (first 6 h) response to endotoxin. Therefore ANF should be considered as a potential mediator of renal and hemodynamic changes induced by sepsis. It is difficult to determine if ANF elevation is an epiphenomenon or a causative factor, because no antagonist of ANF is currently available.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Hyperosmolality elevates plasma atrial natriuretic factor in the ovine fetus

1989 ◽  
Vol 257 (4) ◽  
pp. E466-E472 ◽  
Author(s):  
C. Y. Cheung ◽  
L. K. Miner ◽  
R. A. Brace
Keyword(s):  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Osmolality ◽  
Hypertonic Solution ◽  
Vascular Volume ◽  
Fetal Plasma ◽  
Natriuretic Factor ◽  
Ovine Fetus ◽  
Pressure Changes ◽  
Atrial Natriuretic

This study was designed to explore the effect of hyperosmolality on fetal plasma atrial natriuretic factor (ANF) concentrations in chronically catheterized sheep fetuses averaging 133 days gestation. An isotonic solution of 0.9% NaCl or hypertonic solution of 2.5% NaCl, 13% mannitol, or 7% NaCl was infused intravascularly into the fetuses at 20 ml/kg over 10 min and simultaneously into their mothers. Fetal plasma osmolality changed by -2 +/- 1 (SE) mosmol/kg in the isotonic group and by 16 +/- 2, 20 +/- 4, and 56 +/- 3 mosmol/kg in the 2.5% NaCl, 13% mannitol, and 7% NaCl groups, respectively (P less than 0.00001). Preinfusion fetal ANF levels were similar in all four groups and averaged 145 +/- 7 (SE) pg/ml. With infusion, fetal plasma ANF increased significantly in the isotonic group by 28 +/- 6%. In the 2.5% NaCl and 13% mannitol groups, the increment in plasma ANF was four times, whereas in the 7% NaCl group it was eight times that in the isotonic group (P less than 0.01). Blood volume and venous pressure changes were similar in all groups. In the hypertonic groups, plasma ANF and venous pressure returned to control levels within 1 h after the start of the infusion, whereas plasma osmolalities remained elevated. Thus infusions of hypertonic solutions into the ovine fetus caused much greater increases in plasma ANF concentrations compared with those seen with isotonic infusion. The return of plasma ANF levels to control despite maintained hyperosmolality suggests that hyperosmolality stimulated ANF release either by a direct but transient mechanism or by potentiating the effects of vascular volume expansion.

Hemodynamic Effects of Atrial Natriuretic Factor Clearance Receptor Occupancy in Conscious Sheep

1990 ◽  
Vol 3 (11) ◽  
pp. 829-832 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. A. Lewicki ◽  
R. M. Scarborough ◽  
B. A. Scoggins
Keyword(s):  
Atrial Natriuretic Factor ◽  
Receptor Occupancy ◽  
Hemodynamic Effects ◽  
Natriuretic Factor ◽  
Clearance Receptor ◽  
Conscious Sheep ◽  
Atrial Natriuretic
Sign in / Sign up

Export Citation Format

Share Document