Determinants of Plasma Atrial Natriuretic Factor (ANF) in Chronic Renal Failure

1988 ◽  
Vol 75 (s19) ◽  
pp. 48P-48P
Author(s):  
AS Woolf ◽  
JC Kingswood ◽  
A Kumar ◽  
TL Lyon ◽  
MA Mansell ◽  
...  
1989 ◽  
Vol 7 ◽  
pp. S238-239 ◽  
Author(s):  
Giancarlo Tonolo ◽  
Aldo Soro ◽  
V. Scardaccio ◽  
Chiara Troffa ◽  
Antonio Pazzola ◽  
...  

1995 ◽  
Vol 269 (3) ◽  
pp. H902-H908 ◽  
Author(s):  
J. K. Luk ◽  
E. F. Wong ◽  
N. L. Wong

Studies were performed to examine the changes of renal ANF second messenger guanosine 3',5'-cyclic monophosphate (cGMP) responses and receptor properties in chronic renal failure (CRF). Five-sixths-nephrectomized and sham-operated Wistar rats were used. The glomerular filtration rate was decreased in the five-sixths-nephrectomized rats, which also had significantly higher plasma blood urea nitrogen and plasma atrial natriuretic factor (ANF) levels (148.5 +/- 10.2 vs. 115.7 +/- 7.3 pg/ml, P = 0.01) than the sham rats. In vitro ANF-stimulated cGMP accumulations in glomeruli of five-sixths-nephrectomized rats were higher than controls. Radioligand-binding experiments showed downregulation of the total ANF receptor in both acid and nonacid wash CRF glomeruli (nonacid wash: 189 +/- 25 vs. 362.8 +/- 52.8 fmol/mg protein, P < 0.05; acid wash: 449.8 +/- 67 vs. 652.7 +/- 52.5 fmol/mg protein, P < 0.05). No change in receptor densities was observed in the des(Gln18,Ser19,Gly20,Leu21)atrial natriuretic peptide-(4--23)-NH2-resistant receptors between sham and CRF rat glomeruli. Therefore, downregulation of ANF clearance receptors exists in CRF rat glomeruli, and this is associated with the exaggerated ANF-stimulated cGMP response in these CRF glomeruli. Hypersensitivity of CRF rat to ANF, together with high plasma ANF levels and downregulation of clearance receptor, may contribute to increased sodium excretion in CRF.


1993 ◽  
Vol 84 (1) ◽  
pp. 31-39 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
M. N. Peraldi ◽  
J. M. Lecomte ◽  
C. Gros ◽  
...  

1. The acute effects of a single oral dose of sinorphan (100 mg), an inhibitor of neutral endopeptidase, on the plasma atrial natriuretic factor level and the fractional excretion of sodium were examined in 12 patients with severe chronic renal failure who were not on maintenance haemodialysis and who ingested a normal sodium diet. The drug was administered against placebo by a double-blind cross-over protocol. 2. Basal plasma atrial natriuretic factor level and fractional excretion of sodium were high (23.2 ± 3.7 pmol/l and 2.64 ± 0.38%, respectively). Sinorphan inhibited plasma neutral endopeptidase activity by 68–75% 30 min after ingestion. This effect persisted for at least 4 h. There were simultaneously increases in plasma atrial natriuretic factor and cyclic GMP levels to 1.9 and 1.4 times the basal values, respectively. Fractional excretion of sodium increased during the second and third hour periods after ingestion of the drug with a peak of 1.9 times the basal value in the second period. Changes in fractional excretion of sodium were significantly correlated with those in plasma atrial natriuretic factor and cyclic GMP levels. Plasma aldosterone level, creatinine clearance and mean blood pressure were unchanged, whereas plasma renin activity increased slightly. An increase in urinary cyclic GMP excretion was observed in parallel with the increase in plasma cyclic GMP level. 3. The results of the present study indicate that (i) high basal values of plasma atrial natriuretic factor level and fractional excretion of sodium, as observed in patients with chronic renal failure, are associated with marked effects of neutral endopeptidase inhibition; (ii) fractional sodium excretion increases after protection of endogenous atrial natriuretic factor from degradation independently of any initial change in extracellular fluid volume or sodium intake, which suggests that this hormone may play a role in the control of sodium excretion in chronic renal failure.


1987 ◽  
Vol 14 (3) ◽  
pp. 247-251 ◽  
Author(s):  
G. P. Hodsman ◽  
B. Jackson ◽  
L. M. Debrevi ◽  
K. Ogawa ◽  
C I. Johnston

1989 ◽  
Vol 65 (764) ◽  
pp. 362-366 ◽  
Author(s):  
A. S. Woolf ◽  
M. A. Mansell ◽  
B. I. Hoffbrand ◽  
S. L. Cohen ◽  
P. J. Moult

1990 ◽  
Vol 78 (3) ◽  
pp. 327-334 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
J. P. Wolf ◽  
S. Czekalski ◽  
F. Mignon ◽  
...  

1. In order to examine the potential role of atrial natriuretic factor in modulating the increased sodium excretion per nephron in chronic renal failure, we studied 12 uraemic patients on the last day of two successive 7 day periods during which their sodium intake was 100 and 20 mmol of sodium/day, respectively. 2. There was a parallel decrease from 6.31 ± 0.75 to 2.17 ± 0.32% in the fractional excretion of filtered sodium and from 234.4 ± 74.9 to 80.6 ± 20.3 pg/ml (supine position) or 140.1 ± 43.6 to 60.7 ± 14.6 pg/ml (upright position) in plasma atrial natriuretic factor. Both parameters were significantly correlated during the two periods of different sodium intake (P <0.05). The ratio of plasma guanosine 3′:5′-cyclic monophosphate to plasma creatinine changed proportionally to plasma atrial natriuretic factor. Plasma aldosterone and plasma renin activity increased during the sodium-depleted period but only plasma renin activity was significantly correlated with fractional excretion of filtered sodium. 3. The predominant role of atrial natriuretic factor compared with that of aldosterone in the renal response to varying sodium intake is suggested both by regression analysis and by the effect of 5 day's treatment with a converting enzyme inhibitor (enalapril) in six other uraemic patients on a normal (100 mmol/day) sodium intake. Such treatment, although resulting in a significant increase in plasma renin activity and a significant decrease in plasma aldosterone, at least in the supine position, did not modify the fractional excretion of sodium and plasma atrial natriuretic factor. 4. Taken together, these results suggest a role for plasma atrial natriuretic factor in promoting the adaptation of sodium excretion on chronic changes of sodium intake in patients with chronic renal failure.


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