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Serum proatrial natriuretic peptide does not increase with higher systolic blood pressure in obese men
  1. Camilla L Asferg1,
  2. Ulrik B Andersen1,
  3. Allan Linneberg2,3,4,
  4. Paula L Hedley5,
  5. Michael Christiansen5,
  6. Jens P Goetze6,
  7. Jørgen L Jeppesen4,7
  1. 1Department of Clinical Physiology, Rigshospitalet Glostrup, University of Copenhagen, Glostrup, Denmark
  2. 2Research Centre for Prevention and Health, the Capital Region of Denmark, Copenhagen, Denmark
  3. 3Department of Clinical Experimental Research, Rigshospitalet, University of Copenhagen, Glostrup, Denmark
  4. 4Faculty of Health and Medical Sciences, University of Copenhagen, Denmark
  5. 5Department of Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark
  6. 6Department of Clinical Chemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
  7. 7Department of Medicine, Amager Hvidovre Hospital Glostrup, University of Copenhagen, Glostrup, Denmark
  1. Correspondence to Dr Camilla Asferg Department of Clinical Physiology, Rigshospitalet Glostrup, University of Copenhagen, Ndr. Ringvej, Glostrup DK-2600, Denmark; c.asferg{at}gmail.com

Abstract

Objective Obese persons have low circulating natriuretic peptide (NP) concentrations. It has been proposed that this ‘natriuretic handicap’ could play a role in obesity-related hypertension. The normal physiological response of the NP system to an increase in blood pressure (BP) is an increase in NP secretion with concomitant higher circulating NP concentrations. In this study, we investigated whether higher BP would also be related to higher circulating NP concentrations in obese men; furthermore, we verified that BP had affected the hearts of our study participants, by determining left ventricular mass (LVM).

Methods We examined 103 obese healthy medication-free men. We measured 24-hour ambulatory BP (ABP). LVM was calculated using the Cornell voltage-duration product method. Fasting serum concentrations of midregional proatrial NP (MR-proANP), a surrogate for active ANP, were measured. Linear regression analysis was used to calculate age-adjusted standardised regression coefficients (β).

Results LVM and BP increased across systolic ABP quartiles (mean LVM±SD: 1599.1±387.2 mm ms in first vs 2188.5±551.3 mm ms in fourth quartile, p<0.001; mean systolic ABP±SD: 114.5±4.2 mm Hg in first vs 149.0±7.7 mm Hg in fourth quartile, p<0.001). Systolic ABP was robustly associated with LVM (ß=0.48, p<0.001). Despite evidence of BP-related increases in LVM, serum MR-proANP was negatively associated with systolic ABP (ß=−0.32, p=0.004) and with diastolic ABP (ß=−0.45, p<0.001).

Conclusions Contrary to known physiological BP responses, MR-proANP was negatively associated with ABP in our study. This suggests that a low amount of circulating NPs could play a role in the early stage of obesity-related hypertension.

  • ECG/electrocardiogram

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Footnotes

  • Contributors CLA designed, planned, and conducted the study, performed the statistical analyses and participated in writing the manuscript. UBA participated in conducting the study and in writing the manuscript. AL participated in recruiting study participants and in writing the manuscript. PLH, MC and JPG participated in measuring MR-proANP and BNP and in writing the paper. JLJ participated in designing, planning and writing the study.

  • Funding This study was funded by grants from the Danish Heart Foundation and the Novo Nordisk Foundation.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval The study was approved by the Danish Ethical Committee (HB-2007–040).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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