Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension

The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP1–30 and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30 (668±330 versus 358±150 pmol/L;P <0.00001) and urodilatin (18.7±5.2 versus 16.0±8.3 pmol/24 h;P <0.05). ProANP1–30 correlated with salt sensitivity at baseline (r =0.76, P <0.000001), after the low- (r =0.80, P <0.0000001) and high-salt diets (r =0.85, P <0.00000001). The increase in proANP1–30 induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r =0.78, P <0.000001). ProANP1–30 was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r =0.58, P <0.01) and after the high-salt diet (r =0.62, P <0.001). In conclusion, the close correlations between proANP1–30 and salt sensitivity suggest that proANP1–30 may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.