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Am J Physiol Heart Circ Physiol 291: H1529-H1535, 2006. First published April 28, 2006; doi:10.1152/ajpheart.00107.2006
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Lack of activation of molecular forms of the BNP system in human grade 1 hypertension and relationship to cardiac hypertrophy

Paola Belluardo,1 Alessandro Cataliotti,1,2 Lorena Bonaiuto,1 Eliana Giuffrè,1 Egle Maugeri,1 Paola Noto,1 Giovanna Orlando,1 Giuseppa Raspa,1 Brigida Piazza,1 Luciano Babuin,2 Horng H. Chen,2 Fernando L. Martin,2 Paul M. McKie,2 Denise M. Heublein,2 John C. Burnett, Jr.,2 and Lorenzo S. Malatino1

1Department of Medicine, University of Catania, Catania, Italy; and 2Cardiorenal Research Laboratory, Mayo Clinic, Rochester, Minnesota

Submitted 30 January 2006 ; accepted in final form 18 April 2006

We evaluated relationships among two circulating molecular forms of brain natriuretic peptide (BNP32 and NT-proBNP), severity of hypertension (HTN), and cardiac hypertrophy in subjects with mild, moderate, and severe HTN. We prospectively studied 78 patients (43 males; mean age 51.4 ± 11 yr) with essential HTN and 28 age- and sex-matched controls. BNP32 and NT-proBNP were measured by radioimmunoassay. In grade 1 HTN, BNP32 was not elevated and NT-proBNP was reduced (P = 0.030) compared with controls. However, log-transformed values of BNP32 and NT-proBNP were both increased with severity of HTN from grade 1 to 3 (P <0.0001 and P = 0.003, respectively). By multivariate analysis, log BNP32 was independently predicted by age (beta = 0.210, P = 0.026) and HTN grade (beta = 0.274, P = 0.004), whereas log NT-proBNP was independently predicted by sex (beta = 0.235, P = 0.012) and HTN grade (beta = 0.218, P = 0.0023). Two forms of BNP were measured in normal subjects and patients with essential HTN. In grade 1 HTN, BNP32 was unchanged and NT-proBNP was significantly reduced compared with controls. As severity increased in humans with grade 1 to 3 HTN, both BNP32 and NT-proBNP levels were increased while not being affected by the presence of left ventricular hypertrophy. The lack of activation of BNP32 together with the reduction of NT-proBNP in grade 1 HTN may represent an impaired response of the BNP system in the early phase of HTN. The later activation of both forms of BNP may be a late compensatory effect, because it correlates with severity of HTN rather than cardiac hypertrophy/remodeling.

natriuretic peptide; brain natriuretic peptide; amino-terminal pro-brain natriuretic peptide; left ventricular hypertrophy



Address for reprint requests and other correspondence: A. Cataliotti, Cardiorenal Research Laboratory, 200 First St., SW, Rochester, MN 55905 (e-mail: cataliotti.alessandro{at}mayo.edu)




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