Clearance receptor-mediated control of atrial natriuretic factor in experimental congestive heart failure

1994 ◽  
Vol 266 (3) ◽  
pp. R936-R943
Author(s):  
R. R. Brandt ◽  
M. M. Redfield ◽  
L. L. Aarhus ◽  
J. A. Lewicki ◽  
J. C. Burnett
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Urinary Sodium Excretion ◽  
Control Group ◽  
Chronic Congestive Heart Failure ◽  
Group Of Seven ◽  
Natriuretic Factor ◽  
Clearance Receptor ◽  
Atrial Natriuretic

Circulating atrial natriuretic factor (ANF) is regulated by clearance receptors (ANFR-C). C-ANF-(4-23) is a ring-deleted analogue of ANF, which binds specifically to ANFR-C. The present studies were undertaken to determine total metabolic (TMCR), pulmonary (PCR), and renal clearance rates (RCR) of ANF in a group of seven mongrel dogs in chronic congestive heart failure (CHF) in comparison with a control group (n = 6). TMCR was not altered in CHF [1,534 +/- 319 vs. control: 1,735 +/- 208 ml/min; P = not significant (NS)] in association with an elevation of circulating endogenous ANF (206 +/- 44 vs. control: 36 +/- 10 pg/ml; P < 0.01). Infusion of C-ANF-(4-23) reduced TMCR in both groups similarly (CHF: 753 +/- 134 vs. control: 972 +/- 156 ml/min; P = NS). PCR was lower in CHF (286 +/- 431 vs. 1,672 +/- 407 ml/min; P < 0.05), whereas RCR was not different (10 +/- 24 vs. control: 15 +/- 25 ml/min; P = NS). ANFR-C blockade did not facilitate urinary sodium excretion in CHF. These studies demonstrate that 1) TMCR does not contribute to elevated endogenous ANF in CHF; 2) total functional activity of the clearance receptor pathway is preserved in CHF; and 3) renal ANF metabolism and the clearance receptor pathway are not linked to the avid sodium retention and renal ANF resistance observed in chronic CHF.

Cardiac secretion of atrial natriuretic factor with exercise in chronic congestive heart failure patients

1992 ◽  
Vol 73 (4) ◽  
pp. 1637-1643 ◽  
Author(s):  
R. J. Cody ◽  
S. H. Kubo ◽  
J. H. Laragh ◽  
S. A. Atlas
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Right Ventricular ◽  
Atrial Natriuretic Factor ◽  
Physiological Stress ◽  
Right Atrial ◽  
Peak Exercise ◽  
Chronic Congestive Heart Failure ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

We have previously reported a fivefold increase of plasma atrial natriuretic factor (ANF) in patients with congestive heart failure (CHF) compared with normal subjects. However, given the marked increase of ANF under basal conditions, the extent to which ANF secretion can further increase under physiological stress is not been clarified in CHF. We therefore evaluated ANF secretion during ergometric exercise in 11 patients with CHF, with peripheral venous ANF samples obtained at rest and peak exercise. In seven patients, simultaneous peripheral venous and right ventricular ANF samples were obtained to estimate myocardial ANF secretion. Hemodynamic characteristics of exercise included a significant increase of heart rate, mean arterial pressure, and cardiac output (all P < 0.01); reduction of systemic vascular resistance (P < 0.001); and increase of right atrial and pulmonary wedge pressures (P < 0.001). ANF was abnormally elevated at baseline (108 +/- 58 fmol/ml) yet increased further to 183 +/- 86 fmol/ml with exercise (P < 0.003). A step-up of right ventricular ANF, particularly during exercise, was consistent with active myocardial secretion, despite elevated baseline ANF levels.

Biologic role of atrial natriuretic factor clearance receptor in congestive heart failure

1993 ◽  
Vol 265 (1) ◽  
pp. H401-H408 ◽  
Author(s):  
M. A. Perrella ◽  
L. L. Aarhus ◽  
D. M. Heublein ◽  
J. A. Lewicki ◽  
J. C. Burnett
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Neutral Endopeptidase ◽  
Amino Acid Peptide ◽  
Natriuretic Factor ◽  
Anesthetized Dogs ◽  
Clearance Receptor ◽  
Atrial Natriuretic

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)

Restoration of renal response to atrial natriuretic factor in experimental low-output heart failure

1989 ◽  
Vol 257 (4) ◽  
pp. R917-R923 ◽  
Author(s):  
M. M. Redfield ◽  
B. S. Edwards ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Vena Cava ◽  
Control Group ◽  
Chronic Congestive Heart Failure ◽  
Relative Role ◽  
Ang Ii ◽  
Renal Response ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The renal response to atrial natriuretic factor (ANF) has been shown to be blunted in several experimental models of acute and chronic congestive heart failure. The mechanism responsible for this blunted response has been postulated to be activation of the renin-angiotensin system with associated potent antinatriuretic effects and/or the reduction in renal perfusion pressure (RPP) characteristic of heart failure. The present study was designed to examine the relative role of these two factors in mediating the blunted response to ANF in a model of acute low output heart failure produced by thoracic inferior vena cava constriction (TIVCC) in the anesthetized dog. TIVCC was produced in five groups of dogs. In group 1, ANF was infused after TIVCC to document the blunted natriuretic response. In group 2, ANF was infused after TIVCC in the presence of blockade of intrarenal angiotensin II (ANG II) by the intrarenal infusion of saralasin (Sar) at a dose without systemic effects. In group 3, ANF was infused after TIVCC in the presence of restoration of RPP by infusion of ANG II at a dose titrated to restore RPP to the level present before TIVCC. In group 4, ANF was infused in the presence of restoration of RPP with ANG II and blockade of intrarenal ANG II with Sar. Group 5 served as an additional control group where the effect of ANG II and Sar in TIVCC was examined in the absence of ANF. Restoration of RPP but not blockade of intrarenal ANG II resulted in a restoration of the response of sodium excretion and glomerular filtration rate to ANF. ANG II plus Sar in the absence of ANF did not produce a natriuresis. We conclude that RPP, more than intrarenal ANG II, modulates the blunted renal response to ANF observed in this model of acute low-output heart failure.

scholarly journals Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure.

1993 ◽  
Vol 4 (2) ◽  
pp. 162-167
Author(s):  
D L Fett ◽  
P G Cavero ◽  
J C Burnett
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Low Dose ◽  
Control Group ◽  
Natriuretic Factor ◽  
Group 2 ◽  
Humoral Responses ◽  
Atrial Natriuretic

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

Cardiac and Plasma Atrial Natriuretic Factor in Experimental Congestive Heart Failure*

Endocrinology ◽  
1987 ◽  
Vol 121 (1) ◽  
pp. 248-257 ◽  
Author(s):  
JINFENG DING ◽  
GAÉTAN THIBAULT ◽  
JOLANTA GUTKOWSKA ◽  
RAUL GARCIA ◽  
THEODORE KARABATSOS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Atrial Natriuretic
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