Plasma brain natriuretic peptide and N-terminal proatrial natriuretic peptide levels in obese patients: a cause or result of hypertension?

Proatrial Natriuretic Peptide Levels in Obese Patients: A Cause or Result of Hypertension? To the Editor: We read with great interest the paper by Wang et al1 indicating that obese subjects had lower brain natriuretic peptide (BNP) and N-terminal proatrial natriuretic peptide (N-terminal proANP) levels than did lean subjects in a large sample population of the Framingham Heart Study. They speculated that lower BNP levels might result from increased receptors in adipose tissue and that lower natriuretic peptide levels might predispose obese patients to hypertension. Their results are interesting; however, we question the hypotheses derived from their cross-sectional, observational study. In that study, not only BNP, but also N-terminal proANP was decreased in obese patients, strongly suggesting decreased release of natriuretic peptides from the heart. In addition, a higher proportion of overweight and obese patients received antihypertensive therapy, as compared with patients who had a normal body mass index. The production of natriuretic peptide is known to be affected by medical treatment, including antihypertensive drugs and statins. Furthermore, whether very small differences in natriuretic peptide levels ( 5 ng/L) between obese and lean subjects contribute to the development of hypertension is questionable, despite evidence showing that complete gene disruption of the natriuretic peptide system causes hypertension in mice. Confirmation of the effects of obesity on plasma natriuretic peptide levels would require prospective and interventional studies examining whether reduction in body weight modifies natriuretic peptide levels. We recently investigated the effects of a hypocaloric diet on plasma natriuretic peptide levels in 12 obese patients with essential hypertension (age, 48 to 81 years; body mass index, 26 to 34 kg/m).2 A standard diet of 2000 kcal/d was given for 1 week, followed by a hypocaloric diet of 850 kcal/d for 3 weeks. Sodium intake remained constant. The patients lost 3.7 0.2 (mean SE) kg of body weight during the hypocaloric diet period (P 0.0001), accompanied by a reduction in systolic blood pressure (10.3 3.6 mm Hg, P 0.02). Plasma BNP and ANP levels decreased significantly from 22.7 5.7 to 16.7 4.5 ng/L and from 22.2 5.0 to 13.4 2.1 ng/L, respectively (P 0.04 for each). McMurray and Vesely3 also confirmed a dramatic fall in plasma ANP levels after 12 weeks of weight reduction in both obese normotensive and hypertensive subjects. Messaoudi et al4 reported that a very low-calorie diet with a constant sodium intake decreased plasma ANP levels in 12 obese subjects over the course of 8 days. Taken together, these observations suggest that obesity may be associated with plasma volume expansion accompanied by elevated natriuretic peptide levels. Even in obese patients with hypertension, natriuretic peptides may protect against further elevation of blood pressure rather than contribute to the pathogenesis of hypertension.