scholarly journals Role of endogenous atrial natriuretic factor in acute congestive heart failure.

1989 ◽  
Vol 84 (6) ◽  
pp. 1962-1966 ◽  
Author(s):  
M E Lee ◽  
W L Miller ◽  
B S Edwards ◽  
J C Burnett
1993 ◽  
Vol 265 (1) ◽  
pp. H401-H408 ◽  
Author(s):  
M. A. Perrella ◽  
L. L. Aarhus ◽  
D. M. Heublein ◽  
J. A. Lewicki ◽  
J. C. Burnett

Atrial natriuretic factor (ANF) is a circulating 28-amino acid peptide that functions in the regulation of sodium homeostasis and vascular tone. ANF metabolism occurs via degradation by neutral endopeptidase 24.11 and binding to the ANF clearance receptor (ANFR-C). The present study was performed on anesthetized dogs, normal (control) and with experimental congestive heart failure (CHF), and was designed to investigate the ability of an ANF ligand specific for ANFR-C [C-ANF-(4-23)] to increase plasma ANF and also to evaluate the influence of ANFR-C on regional pulmonary and renal ANF clearances. C-ANF-(4-23) increased plasma ANF in controls (51 +/- 15 to 123 +/- 39 pg/ml; P < 0.05) and further increased plasma ANF in CHF dogs (242 +/- 30 to 327 +/- 34; P < 0.05), demonstrating that ANFR-C plays a significant role in the overall metabolism and clearance of ANF, even with chronically elevated ANF. Infusion of C-ANF-(4-23) produced a marked decrease in ANF pulmonary clearance (PCLANF) in controls (1,018 +/- 405 to -286 +/- 383 ml/min; P < 0.05); however, PCLANF was not altered by the ANF ligand in CHF dogs [-137 +/- 174 to -106 +/- 226 ml/min; not significant (NS)], suggesting an occupancy of ANFR-C or a downregulation of this receptor with chronically elevated plasma ANF. ANF renal clearance (RCLANF) was not altered in either group by C-ANF-(4-23) infusion.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 65 (8) ◽  
pp. 1706-1711 ◽  
Author(s):  
C. I. Johnston ◽  
L. F. Arnolda ◽  
K. Tsunoda ◽  
P. A. Phillips ◽  
G. P. Hodsman

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.


Endocrinology ◽  
1987 ◽  
Vol 121 (1) ◽  
pp. 248-257 ◽  
Author(s):  
JINFENG DING ◽  
GAÉTAN THIBAULT ◽  
JOLANTA GUTKOWSKA ◽  
RAUL GARCIA ◽  
THEODORE KARABATSOS ◽  
...  

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