Atrial natriuretic factor and changes in dietary sodium intake in patients with chronic renal failure

1990 ◽  
Vol 78 (3) ◽  
pp. 327-334 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
J. P. Wolf ◽  
S. Czekalski ◽  
F. Mignon ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Renin Activity ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

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.

Inhibition of neutral endopeptidase stimulates renal sodium excretion in patients with chronic renal failure

1993 ◽  
Vol 84 (1) ◽  
pp. 31-39 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
M. N. Peraldi ◽  
J. M. Lecomte ◽  
C. Gros ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cyclic Gmp ◽  
Atrial Natriuretic Factor ◽  
Fractional Excretion ◽  
Neutral Endopeptidase ◽  
Factor Level ◽  
Natriuretic Factor ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

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.

Atrial natriuretic factor: reduced cardiac content in cirrhotic rats with ascites

1986 ◽  
Vol 250 (4) ◽  
pp. F749-F752 ◽  
Author(s):  
W. Jimenez ◽  
A. Martinez-Pardo ◽  
V. Arroyo ◽  
J. Gaya ◽  
F. Rivera ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Urine Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Natriuretic Factor ◽  
Tissue Content ◽  
Atrial Natriuretic

The present study was designed to investigate whether cirrhosis with ascites is associated with altered tissue content of atrial natriuretic factor. Atrial extracts from 14 cirrhotic rats with ascites and increased plasma renin activity (PRA) (14.4 +/- 4.6 ng X ml-1 X h-1) and aldosterone concentration (148.3 +/- 17.3 ng/dl) and from 10 control rats (PRA, 3 +/- 0.5 ng X ml-1 X h-1; aldosterone, 34.7 +/- 3.7 ng/dl) were intravenously injected into anesthetized normovolemic rats. Only one extract was assayed in each bioassay rat. Atrial extracts from control rats increased diuresis and natriuresis 513 +/- 91 and 3,029 +/- 752%, respectively (means +/- SE). In contrast, atrial extracts from cirrhotic rats increased urine volume 199 +/- 49% (P less than 0.001) and sodium excretion 546 +/- 132% (P less than 0.001). These results strongly suggest that atrial content of atrial natriuretic factor is reduced in cirrhotic rats as compared with control animals.

Atrial Natriuretic Factor Attenuates Prostaglandin E2-Stimulated Plasma Renin Activity in Humans

1989 ◽  
Vol 14 (2) ◽  
pp. 326-330 ◽  
Author(s):  
John McMurray ◽  
Lesley McFarlane ◽  
Wendy Coutie ◽  
David Balfour ◽  
Allan Struthers
Keyword(s):  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Aldosterone and renin inhibition by physiological levels of atrial natriuretic factor

1988 ◽  
Vol 254 (6) ◽  
pp. R1011-R1016 ◽  
Author(s):  
M. W. Brands ◽  
R. H. Freeman
Keyword(s):  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Base Line ◽  
Lower Plasma ◽  
Aldosterone Secretion ◽  
Low Sodium Diet ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

This study was designed to examine, in the rat, the inhibition of renin release and aldosterone secretion by physiological plasma levels of atrial natriuretic factor (ANF). Intravascular volume expansion over 30 min with donor blood equal to 3% body weight increased plasma ANF concentration from a base line of 216 +/- 28 to 1,590 +/- 240 pg/ml (P less than 0.001) in sodium-replete rats. Basal plasma ANF levels were decreased to 125 +/- 9 pg/ml in animals fed a low-sodium diet, and the infusion of synthetic ANF into separate groups of these rats at doses of 15 or 45 ng.kg-1.min-1 elevated plasma ANF to 346 +/- 38 and 720 +/- 96 pg/ml, respectively (P less than 0.001 for both values). Infusion of ANF at 15 ng.kg-1.min-1 resulted in a significantly lower plasma renin activity [30 +/- 3 vs. 69 +/- 5 ng angiotensin I (ANG I).ml-1.h-1, P less than 0.05], but there was no difference in aldosterone secretion between control and infused groups (7.00 +/- 0.49 vs. 7.29 +/- 0.95 ng/min, P greater than 0.05). However, the higher ANF dose of 45 ng.kg-1.min-1 did reduce aldosterone secretion approximately 40% to 4.18 +/- 0.36 ng/min (P less than 0.001) with no further suppression in plasma renin activity. In sodium-replete rats, infusion of ANF at 45 ng.kg-1.min-1 resulted in lower plasma renin activity compared with the control noninfused group (14 +/- 4 vs. 22 +/- 2 ng ANG I.ml-1.h-1, P less than 0.05), but aldosterone secretion was not different (P greater than 0.05) between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of Atrial Natriuretic Factor in Changes in the Responsiveness of Aldosterone to Angiotensin II Secondary to Sodium Loading and Depletion in Man

1990 ◽  
Vol 79 (1) ◽  
pp. 57-65 ◽  
Author(s):  
H. Tuchelt ◽  
G. Eschenhagen ◽  
V. Bähr ◽  
G. Schwietzer ◽  
H. M. Thiede ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Depletion ◽  
Natriuretic Factor ◽  
Sodium Loading ◽  
Atrial Natriuretic

1. Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. The hypothesis was tested that these changes in responsiveness of the zona glomerulosa are mediated in part by changes in plasma atrial natriuretic factor levels. 2. To this end, plasma renin activity and plasma aldosterone were measured in the upright and recumbent position and during incremental infusions of angiotensin II (1, 3 and 6 ng of angiotensin II amide min−1 kg−1 for 1 h each dose) after 6 days of sodium loading (study 1), after 5 days of sodium depletion (study 2) and after sodium depletion plus infusion of atrial natriuretic factor (0.13 μg/min for 8 h) on the test day (study 3). Six normal young males were investigated. 3. Plasma atrial natriuretic factor levels were around 5 pmol/l in study 2, 15 pmol/l in study 1 and 15 pmol/l in study 3 during infusion of atrial natriuretic factor. Two hours after the onset of atrial natriuretic factor infusion, plasma renin activity and plasma aldosterone (recumbent) were markedly and significantly lower in study 3 than in study 2, but still significantly higher than in study 1. The increase in plasma aldosterone after infusion of angiotensin II was slightly, but not significantly, blunted by infusion of atrial natriuretic factor in study 3 compared with study 2. The overall increase in plasma aldosterone was still significantly greater in study 3 than in study 1. 4. The fall in renal plasma flow, determined as p-aminohippurate clearance, during infusion of angiotensin II was greater in study 1 than in studies 2 and 3. Small differences between study 3 and study 2 were not significant. 5. It is concluded that infusions of atrial natriuretic factor in the low-sodium state that mimic plasma atrial natriuretic factor levels after sodium loading lead to a marked fall in recumbent plasma aldosterone, which is to a large extent secondary to a fall in plasma renin activity. A small direct effect of these physiologically elevated atrial natriuretic factor levels on the zona glomerulosa itself (the increase in plasma aldosterone during angiotensin II infusion) was only of borderline significance. Thus, atrial natriuretic factor at physiological plasma concentrations is a regulator of renin and aldosterone secretion, whereas a modulating effect on the renal vasoconstrictor action of angiotensin II could not be demonstrated.

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