Inefficacy of daily single bolus dose atrial natriuretic factor in chronic congestive heart failure

1989 ◽  
Vol 64 (14) ◽  
pp. 948-950 ◽  
Author(s):  
Ian G. Crozier ◽  
A.Mark Richards ◽  
M.Gary Nicholls ◽  
Eric A. Espiner ◽  
Hamid Ikram
1992 ◽  
Vol 73 (4) ◽  
pp. 1637-1643 ◽  
Author(s):  
R. J. Cody ◽  
S. H. Kubo ◽  
J. H. Laragh ◽  
S. A. Atlas

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.


1994 ◽  
Vol 266 (3) ◽  
pp. R936-R943
Author(s):  
R. R. Brandt ◽  
M. M. Redfield ◽  
L. L. Aarhus ◽  
J. A. Lewicki ◽  
J. C. Burnett

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.


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

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