American Journal of Hypertension 31(6) June 2018 645 ORIGINAL ARTICLE Atrial natriuretic peptide (ANP) is well known for its natri- uretic, diuretic, and vasodilatory properties and plays a major role in the regulation of blood volume and blood pressure. 1 Obese persons have lower circulating concentrations of ANP, 2 and it has been proposed that this natriuretic handicap could play a role in obesity-related hypertension. 2,3 In con- trast, it has been observed that hypertensive patients with lef atrial enlargement have higher circulating concentrations of ANP. 4,5 Te relationship between circulating ANP concen- trations and lef atrial size in obese hypertensive patients is, however, unclear. Terefore, the purpose of this study was to investigate whether obese men with hypertension could have lower circulating ANP concentrations despite evidence of blood pressure-induced greater lef atrial size. Te study was designed as an additional echocardiographic substudy to one of our previously published studies. 6 Here we show that considering their high salt intake and high 24-hour ambula- tory blood pressure, obese hypertensive men have lower than expected circulating concentrations of midregional proANP (MR-proANP), a stable marker of ANP secretion, 7 compared with lean normotensive men. 6 Tus, the important novelty of this study relative to our previous published study 6 is the Obese Hypertensive Men Have Lower Circulating Proatrial Natriuretic Peptide Concentrations Despite Greater Left Atrial Size Camilla L. Asferg, 1 Ulrik B. Andersen, 1 Allan Linneberg, 2–4 Jens P. Goetze, 5,6 and Jørgen L. Jeppesen 4,7 BACKGROUND Obese persons have lower circulating natriuretic peptide (NP) concentrations. It has been proposed that this natriuretic handi- cap plays a role in obesity-related hypertension. In contrast, hypertensive patients with left atrial enlargement have higher cir- culating NP concentrations. On this background, we investigated whether obese hypertensive men could have lower circulating NP concentrations despite evidence of pressure-induced greater left atrial size. METHODS We examined 98 obese men (body mass index [BMI] ≥ 30.0 kg/m 2 ) and 27 lean normotensive men (BMI 20.0–24.9 kg/m 2 ). All men were healthy, medication free, with normal left ventricular ejection frac- tion. We measured blood pressure using 24-hour ambulatory blood pressure (ABP) recordings. Hypertension was defned as 24-hour ABP ≥ 130/80 mm Hg, and normotension was defned as 24-hour ABP < 130/80 mm Hg. We determined left atrial size using echocardiog- raphy, and we measured fasting serum concentrations of midregional proatrial NP (MR-proANP). RESULTS Of the 98 obese men, 62 had hypertension and 36 were normoten- sive. The obese hypertensive men had greater left atrial size (mean ± SD: 28.7 ± 6.0 ml/m 2 ) compared with the lean normotensive men (23.5 ± 4.5 ml/m 2 ) and the obese normotensive men (22.7 ± 5.1 ml/m 2 ), P < 0.01. Nevertheless, despite evidence of pressure-induced greater left atrial size, the obese hypertensive men had lower serum MR-proANP concentrations (median [interquartile range]: 48.5 [37.0–64.7] pmol/l) compared with the lean normotensive men (69.3 [54.3–82.9] pmol/l), P < 0.01, whereas the obese normotensive men had serum MR-proANP concentrations in between the 2 other groups (54.1 [43.6–62.9] pmol/l). CONCLUSIONS Despite greater left atrial size, obese hypertensive men have lower circulat- ing MR-proANP concentrations compared with lean normotensive men. Keywords: ambulatory blood pressure; atrial natriuretic peptide; blood pressure; hypertension; left atrial size; natriuretic peptides; proatrial natriuretic peptide. doi:10.1093/ajh/hpy029 Correspondence: Camilla L. Asferg (c.asferg@gmail.com). Initially submitted December 24, 2017; date of frst revision February 10, 2018; accepted for publication February 13, 2018; online publication February 17, 2018. © American Journal of Hypertension, Ltd 2018. All rights reserved. For Permissions, please email: journals.permissions@oup.com 1 Department of Clinical Physiology, Rigshospitalet Glostrup, University of Copenhagen, Glostrup, Denmark; 2 Research Centre for Prevention and Health, The Capital Region of Denmark, Glostrup, Denmark; 3 Department of Clinical Experimental Research, Rigshospitalet Glostrup, University of Copenhagen, Glostrup, Denmark; 4 Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; 5 Department of Clinical Biochemistry, Rigshospitalet Blegdamsvej, University of Copenhagen, Copenhagen, Denmark; 6 Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; 7 Department of Medicine, Amager Hvidovre Hospital Glostrup, University of Copenhagen, Glostrup, Denmark. Downloaded from https://academic.oup.com/ajh/article/31/6/645/4868140 by guest on 25 January 2023