Human Hypertension Is Characterized by a Lack of Activation of the Antihypertensive Cardiac Hormones ANP and BNP
Objectives This study sought to investigate plasma levels of circulating cardiac natriuretic peptides, atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP), in the general community, focusing on their relative differences in worsening human hypertension. Background Although...
Saved in:
Published in | Journal of the American College of Cardiology Vol. 60; no. 16; pp. 1558 - 1565 |
---|---|
Main Authors | , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
16.10.2012
Elsevier Elsevier Limited |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Objectives This study sought to investigate plasma levels of circulating cardiac natriuretic peptides, atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP), in the general community, focusing on their relative differences in worsening human hypertension. Background Although ANP and BNP are well-characterized regulators of blood pressure in humans, little is known at the population level about their relationship with hypertension. The authors hypothesized that hypertension is associated with a lack of activation of these hormones or their molecular precursors. Methods The study cohort (N = 2,082, age >45 years) was derived from a random sample from Rochester, Minnesota, and each subject had a medical history, clinical examination, and assessment of different plasma forms of ANP and BNP. Patients were stratified by blood pressure. Multivariable linear regression was used to assess differences in natriuretic peptide levels in worsening hypertension. Results Compared to normotensive, BNP1–32 and N-terminal proBNP1–76 (NT-proBNP1–76 ) were significantly decreased in pre-hypertension (p < 0.05), with BNP1–32 significantly decreased in stage 1 as well (p < 0.05). Although proBNP1–108 remained unchanged, the processed form was significantly increased only in stage 2 hypertension (p < 0.05). ANP1–28 remained unchanged, while NT-ANP1–98 was reduced in pre-hypertension (p < 0.05). Conclusions The authors demonstrated the existence of an impaired production and/or release of proBNP1–108 along with a concomitant reduction of BNP1–32 and NT-proBNP1–76 in the early stages of hypertension, with a significant elevation only in stage 2 hypertension. Importantly, they simultaneously demonstrated a lack of compensatory ANP elevation in advanced hypertension. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0735-1097 1558-3597 |
DOI: | 10.1016/j.jacc.2012.05.049 |