Relative Atrial Natriuretic Peptide Deficiency and Inadequate Renin and Angiotensin II Suppression in Obese Hypertensive Men

Abstract

Obesity is a strong risk factor for hypertension, but the mechanisms by which obesity leads to hypertension are incompletely understood. On this background, we assessed dietary sodium intake, serum levels of natriuretic peptides (NPs), and the activity of the renin–angiotensin system in 63 obese hypertensive men (obeseHT: body mass index, ≥30.0 kg/m 2 ; 24-hour ambulatory blood pressure, ≥130/80 mm Hg), in 40 obese normotensive men (obeseNT: body mass index, ≥30.0 kg/m 2 ; 24-hour ambulatory blood pressure, <130/80 mm Hg), and in 27 lean normotensive men (leanNT: body mass index, 20.0–24.9 kg/m 2 ; 24-hour ambulatory blood pressure, <130/80 mm Hg). All study subjects were medication free. As a surrogate estimate for dietary sodium intake, we measured sodium excretion in a 24-hour urine collection and we measured serum levels of midregional proatrial NP and plasma levels of renin and angiotensin II. The obese men had higher mean (±SD) urinary sodium excretion (obeseHT, 213.6±85.2 mmol; obeseNT, 233.0±70.0 mmol) than the lean normotensive men (leanNT, 155.5±51.7 mmol; P =0.003). ObeseHT had lower (median [interquartile range]) serum midregional proatrial NP levels (49.2 [37.3–64.7] pmol/L) than leanNT (69.3 [54.3–82.9] pmol/L; P =0.003), whereas obeseNT had midregional proatrial NP levels in between (54.1 [43.2–64.7] pmol/L); obeseNT had lower (median [interquartile range]) plasma levels of renin (5.0 [3.0–8.0] mIU/L versus 9.0 [4.0–18.0]) and angiotensin II (2.4 [1.5–3.5] pmol/L versus 4.2 [2.2–7.9]) than obeseHT ( P ≤0.049), whereas obeseHT had similar plasma levels of renin and angiotensin II as leanNT ( P ≥0.19). Thus, despite a high sodium intake and a high blood pressure, obese hypertensive men have a relative NP deficiency and an inadequate renin–angiotensin system suppression.