Plasma levels of atrial natriuretic peptide are raised in essential hypertension during low and high sodium intake

1987 ◽  
Vol 65 (5) ◽  
pp. 232-237 ◽  
Author(s):  
G. Wambach ◽  
S. Götz ◽  
G. Suckau ◽  
G. Bönner ◽  
W. Kaufmann
1993 ◽  
Vol 85 (1) ◽  
pp. 13-17 ◽  
Author(s):  
G. A. Sagnella ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
D. R. J. Singer ◽  
G. A. MacGregor

1. The present study was designed to investigate the relationships between circulating atrial natriuretic peptide, plasma and urinary cyclic GMP and sodium excretion under basal conditions and in response to changes in dietary sodium intake. 2. Measurements of plasma atrial natriuretic peptide and plasma and urinary (24 h collections) cyclic GMP, sodium and creatinine were made in (i) 30 normotensive subjects on their normal sodium intake and (ii) 12 subjects on the 5th day of a low and on the 5th day of a high sodium intake. 3. Plasma cyclic GMP, urinary cyclic GMP and fractional excretion of cyclic GMP in 30 normotensive subjects on their normal sodium intake were (means ± SEM) 5.4 ± 0.5 pmol/ml, 434.5 ± 31.8 pmol/min and 86.9 ± 8.6%, respectively. There were significant correlations between urinary cyclic GMP and its corresponding filtered load (r = 0.55) and between the renal clearance of cyclic GMP and that of creatinine (r = 0.44), but there were no significant associations between circulating atrial natriuretic peptide and plasma cyclic GMP or the fractional excretion of cyclic GMP or between urinary sodium and the fractional excretion of cyclic GMP. 5. Plasma atrial natriuretic peptide was significantly raised on the 5th day of the high sodium intake compared with the low sodium intake (10.6 ± 1.6 versus 4.2 ± 0.9 pg/ml; P <0.05). Similarly, there were increases in urinary cyclic GMP excretion (692.3 ± 43.4 versus 427.4 ± 41.9 pmol/min, P <0.05), but there were no significant differences in the fractional excretion of cyclic GMP. 6. As neither plasma nor urinary cyclic GMP was strongly associated with circulating levels of atrial natriuretic peptide, the present study suggests that other factors may be more important than circulating atrial natriuretic peptide as determinants of extracellular cyclic GMP.


1987 ◽  
Vol 72 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Nirmala D. Markandu ◽  
Angela C. Shore ◽  
Mary L. Forsling ◽  
Graham A. MacGregor

1. Plasma levels of immunoreactive atrial natriuretic peptide (IrANP), plasma renin activity, aldosterone and vasopressin were measured in 11 normotensive subjects on a low (10 mmol/day), a normal (150 mmol/day) and a high (350 mmol/day) sodium intake. 2. Plasma levels of IrANP increased significantly with increasing dietary sodium intake with levels (means ± sd) of 3.9 ± 2.1 pg/ml on the fifth day of the low sodium diet, 6.1 ± 3.4 pg/ml on the fifth day of the normal sodium diet and 11.4 ± 4.6 pg/ml on the fifth day of the high sodium diet. 3. Plasma renin activity and aldosterone decreased significantly with increasing sodium intake whereas plasma vasopressin was highest on the high sodium intake. 4. These results suggest that the atrial peptides may be a new and important component in the overall control of sodium and water balance during increased sodium intake.


1987 ◽  
Vol 72 (5) ◽  
pp. 531-539 ◽  
Author(s):  
Francesco P. Cappuccio ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Giuseppe A. Sagnella ◽  
Angela C. Shore ◽  
...  

1. Plasma levels of atrial natriuretic peptide (ANP) were measured by radioimmunoassay in eight normal healthy volunteers before and during mineralocorticoid escape. 2. Mean plasma ANP on a fixed sodium intake before fludrocortisone was 6.5± sem 1.1 pg/ml. Within 24 h of fludrocortisone administration there was a significant increase in plasma ANP which continued to increase daily reaching a plateau by day 4 (14.9 ± 2.4 pg/ml) to day 7 (15.1 ± 2.6 pg/ml). 3. The rise in plasma ANP was closely related to the amount of sodium retained during the fludrocortisone treatment and the sodium ‘escape’ occurred by days 4 to 7. 4. These results support the concept that ANP could play an important hormonal role in overcoming the sodium-retaining effects of mineralocorticoids in man.


1990 ◽  
Vol 258 (4) ◽  
pp. F916-F926 ◽  
Author(s):  
A. A. Seymour ◽  
J. N. Swerdel ◽  
S. A. Fennell ◽  
V. J. Kratunis ◽  
M. M. Asaad

Sodium and fluid intake were precisely regulated by 3 days of infusion of 0.07, 0.35, or 3.5 mu eq Na/min at rates of 25, 50, or 100 microliters/min in nine groups of conscious spontaneously hypertensive rats (SHR). At each level of sodium and volume intake, the acute depressor and renal responses to three doses of exogenous atrial natriuretic peptide (ANP)-(99-126) were determined in conscious, unrestrained SHR. The natriuretic responses to the highest dose of ANP-(99-126) (150 pmol/min) were independent of the rate of fluid infusion but were highly dependent on the sodium intake. The maximal increases in sodium excretion averaged 0.9 +/- 0.5 (253%), 2.6 +/- 0.5 (302%), and 15.4 +/- 2.1 mu eq.kg-1.min-1 (577%) in SHR maintained on 0.07, 0.35, and 3.5 mu eq Na/min, respectively. In addition, the diuretic but not the depressor responses to ANP-(99-126) were dependent on the sodium intake and were unrelated to the rate of fluid delivery. In separate groups of SHR, 3 days of infusions of 3.5 mu eq Na/min at 25 and 100 microliters/min significantly elevated plasma ANP from 89 +/- 16 to 200 +/- 60 and 159 +/- 24 fmol/ml, respectively. In conclusion, high sodium intake enhanced the renal responses to exogenous ANP-(99-126) despite increases in endogenous peptide concentrations in conscious SHR.


1987 ◽  
Vol 252 (5) ◽  
pp. R878-R882 ◽  
Author(s):  
J. P. Granger ◽  
J. C. Burnett ◽  
J. C. Romero ◽  
T. J. Opgenorth ◽  
J. Salazar ◽  
...  

Escape from the sodium-retaining effects of aldosterone (ALDO) is thought to occur as a result of natriuretic compensatory mechanisms triggered by extracellular fluid volume expansion. The purpose of the present study was to determine whether increases in plasma levels of atrial natriuretic peptide occur during ALDO escape in conscious dogs (n = 6) maintained on a fixed sodium intake (60 meq/day). Infusion of ALDO at a rate of 15 micrograms X kg-1 X day-1 for 6 days decreased sodium excretion (UNaV) from 59.1 +/- 4.0 to 36.2 +/- 5.7 meq/day on day 1, and then UNaV gradually returned to control levels by day 5 of ALDO infusion. Net cumulative sodium balance progressively increased during ALDO infusion, reaching a peak value of 88.8 +/- 21.3 meq/day on day 5. Mean arterial pressure increased from 85 +/- 3 to 95 +/- 4 mmHg, and plasma renin activity decreased from 1.32 +/- 0.27 to 0.32 +/- 0.07 ng angiotensin (ANG) I X ml-1 X h-1 during ALDO infusion. Plasma levels of atrial natriuretic peptide averaged 67.5 +/- 8.9 pg/ml during control and increased to a peak value of 120 +/- 18 pg/ml by day 4 of ALDO infusion. Three to four days after ALDO infusion was stopped, plasma levels of atrial natriuretic peptide averaged 46 +/- 5 and 50 +/- 6 pg/ml, respectively. In summary, escape from the sodium-retaining effects of ALDO is associated with significant increases in the circulatory levels of atrial natriuretic peptide.


1989 ◽  
Vol 77 (5) ◽  
pp. 573-579 ◽  
Author(s):  
M. G. Buckley ◽  
G. A. Sagnella ◽  
N. D. Markandu ◽  
D. R. J. Singer ◽  
G. A. MacGregor

1. Plasma levels of immunoreactive N-terminal pro-atrial natriuretic peptide (N-terminal ANP) have been measured in 25 normal subjects, 29 patients with essential hypertension, six cardiac transplant recipients, seven patients with dialysis-independent chronic renal failure and 11 patients with haemodialysis-dependent chronic renal failure. Plasma was extracted on Sep-Pak cartridges and N-terminal ANP immunoreactivity was measured using an antibody directed against pro-ANP (1–30). 2. Plasma levels of TV-terminal ANP (means ± sem) were 235.3 ± 19.2 pg/ml in normal subjects and were significantly raised in patients with essential hypertension (363.6 ± 36.3 pg/ml), in cardiac transplant recipients (1240.0 ± 196.2 pg/ml), in patients with chronic renal failure not requiring dialysis (1636.6 ± 488.4 pg/ml) and patients with chronic renal failure on maintenance haemodialysis (10 336.1 ± 2043.7 pg/ml). 3. There were positive and significant correlations between the plasma levels of TV-terminal ANP and α-human ANP (α-hANP) with individual correlation coefficients of 0.68 within the normal subjects, 0.47 in patients with essential hypertension, 0.78 in patients with dialysis-independent chronic renal failure and 0.68 in patients with haemodialysis-dependent chronic renal failure (P < 0.05 in every case). 4. Gel filtration behaviour on Sephadex G-50 of the immunoreactive N-terminal ANP from Sep-Pak extracts of plasma from normal subjects or patients was consistent with a single peak having an elution volume corresponding to that of human pro-ANP (1–67) standard. 5. These studies demonstrate that the N-terminal pro-ANP peptide is co-secreted with α-hANP in both normal subjects and patients with cardiovascular/renal disease. The higher levels of the N-terminal ANP may reflect differences in the rate of elimination from the circulation but the exact structure and functional significance of the circulating N-terminal ANP remains to be established.


1988 ◽  
Vol 154 (2) ◽  
pp. 205-213 ◽  
Author(s):  
TETSUYA NAKAMURA ◽  
SHUICHI ICHIKAWA ◽  
TETSUO SAKAMAKI ◽  
MASAO FUJIE ◽  
ATSUKO MAGI ◽  
...  

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