Abstract

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, …

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