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Hypertension. 2002;39:996-999
doi: 10.1161/01.HYP.0000017552.91014.2A
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(Hypertension. 2002;39:996.)
© 2002 American Heart Association, Inc.


Scientific Contributions

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

Olle Melander; Erik Frandsen; Leif Groop; U. Lennart Hulthén

From the Department of Endocrinology, Lund University (O.M., L.G., U.L.H.), Malmö, Sweden; and the Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital (E.F.), Glostrup, Denmark.

Correspondence to Olle Melander, Department of Endocrinology, Malmö University Hospital MAS, S-205 02 MALMÖ, Sweden. E-mail Olle.Melander{at}endo.mas.lu.se

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.


Key Words: natriuretic peptides • sodium, dietary • hypertension, essential • genetics • blood pressure