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.
