Atrial natriuretic peptide: increased natriuresis in hypertensive vs normotensive subjects

InPharma ◽  
1986 ◽  
Vol 526 (1) ◽  
pp. 6-6
1996 ◽  
Vol 91 (3) ◽  
pp. 293-298 ◽  
Author(s):  
Toshihiko Ishimitsu ◽  
Toshio Nishikimi ◽  
Hiroaki Matsuoka ◽  
Kenji Kangawa ◽  
Kazuo Kitamura ◽  
...  

1. Responses of adrenomedullin to acute and chronic salt loading were examined in normotensive and hypertensive subjects. 2. In the acute salt load study, isotonic saline (50 ml/kg for 1 h) was intravenously infused into nine normotensive subjects and 11 patients with essential hypertension. Plasma adrenomedullin was higher in hypertensive than in normotensive subjects but was unchanged by saline infusion in either the normotensive (before infusion, 2.4 ± 0.2 fmol/ml; after infusion, 2.4±0.1 fmol/ml) or hypertensive (before infusion, 3.0±0.1 fmol/ml; after infusion, 2.9 ± 0.2 fmol/ml) group, while renin was suppressed and atrial natriuretic peptide was markedly increased. Plasma endothelin was not affected either. 3. In the chronic salt load study, seven normotensive subjects and 23 patients with essential hypertension underwent two 7-day periods of 30 and 260 mmol/day sodium intake. Depending on the blood pressure change, 13 hypertensive subjects were classified as salt-resistant and 10 as salt-sensitive. Salt-sensitive hypertensive subjects had suppressed plasma renin activity even during low salt intake. Plasma adrenomedullin or endothelin were not affected by the salt intake changes in any group; however, the high salt intake increased atrial natriuretic peptide in all groups. 4. These data indicate that the circulating level of adrenomedullin is not changed by either acute or chronic salt loading in normotensive subjects and patients with essential hypertension.


1991 ◽  
Vol 81 (s25) ◽  
pp. 509-514 ◽  
Author(s):  
J. Duggan ◽  
S. Kilfeather ◽  
S. L. Lightman ◽  
E. O'Brien ◽  
K. O'Malley

1. Ageing and hypertension are associated with changes in the way in which the body handles sodium. This may involve changes in plasma atrial natriuretic peptide concentration, since atrial natriuretic peptide is a regulator of sodium handling by the kidney and the plasma atrial natriuretic peptide concentration is increased in both ageing and hypertension. An increase in the plasma atrial natriuretic peptide concentration could also be associated with a change in atrial natriuretic peptide receptor density, possibly involving down-regulation. 2. To investigate these possibilities plasma atrial natriuretic peptide concentration and platelet atrial natriuretic peptide binding site density were measured in 18 young, 11 middle-aged and 12 elderly healthy subjects and in 23 patients with mild to moderate essential hypertension. 3. In normotensive subjects, the plasma atrial natriuretic peptide concentration increased with age (r = 0.49, P < 0.01) and was significantly higher in elderly than young subjects (mean ± sem, 31.9 ± 4.5 versus 18.3 ± 2.0 pmol/l, P < 0.05). The plasma atrial natriuretic peptide concentration increased with the mean arterial pressure in normotensive subjects (r = 0.47, P < 0.01). Multiple regression analysis did not show independent relationships between the plasma atrial natriuretic peptide concentration and either age or mean arterial pressure in normotensive subjects alone. However, when normotensive subjects and hypertensive patients were considered together, multiple regression revealed both age and mean arterial pressure as independent predictors of the plasma atrial natriuretic peptide concentration (P < 0.05, P < 0.01, respectively). In normotensive subjects, the platelet atrial natriuretic peptide binding site density did not change with age (r = 0.19, P = 0.27). 4. The plasma atrial natriuretic peptide concentration was elevated in hypertensive patients (37.6 ± 2.5 versus 30.4 ± 3.1 pmol/l, P < 0.05). There was no significant difference in the platelet atrial natriuretic peptide binding site density between hypertensive patients and normotensive subjects. 5. It is concluded that the plasma atrial natriuretic peptide concentration increases with age. The exact mechanism is uncertain, but it may play a role in the altered renal sodium handling seen with age. The elevation in the plasma atrial natriuretic peptide concentration with age is insufficient to induce a secondary reduction in atrial natriuretic peptide binding site density. Similarly, the elevation of the plasma atrial natriuretic peptide concentration in patients with mild to moderate hypertension does not lead to down-regulation of platelet atrial natriuretic peptide binding site density. It appears that increases in circulating atrial natriuretic peptide, greater than those observed in ageing and moderate hypertension, are required to induce down-regulation of platelet atrial natriuretic peptide binding site density.


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.


2001 ◽  
Vol 120 (5) ◽  
pp. A682-A682
Author(s):  
W GOWERJR ◽  
G CARTER ◽  
C LANDON ◽  
W GOWERIII ◽  
J DIETZ ◽  
...  

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