TY - JOUR
T1 - Human hypertension is characterized by a lack of activation of the antihypertensive cardiac hormones ANP and BNP
AU - MacHeret, Fima
AU - Heublein, Denise
AU - Costello-Boerrigter, Lisa C.
AU - Boerrigter, Guido
AU - McKie, Paul
AU - Bellavia, Diego
AU - Mangiafico, Sarah
AU - Ikeda, Yasuhiro
AU - Bailey, Kent
AU - Scott, Christopher G.
AU - Sandberg, Sharon
AU - Chen, Horng H.
AU - Malatino, Lorenzo
AU - Redfield, Margaret M.
AU - Rodeheffer, Richard
AU - Burnett, John
AU - Cataliotti, Alessandro
N1 - Funding Information:
This work was supported by grants from the National Institutes of Health ( RO1 HL36634 , R01-HL55502 , and RO1 HL76611 ), the Stanley J. Sarnoff Endowment for Cardiovascular Science , and the Mayo Division of Cardiology . Funding for this study was also provided in part by Bio-Rad. Dr. Cataliotti was supported by the Doris Duke Charitable Foundation ( CSDA 2006064 ) and by the M.I.U.R. Progetto Rientro dei Cervelli. Dr. Chen has received royalties from Niles Therapeutics, Anexon, and Up-to-Date; and has patent and licensed designer natriuretic peptides with the Mayo Clinic. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
PY - 2012/10/16
Y1 - 2012/10/16
N2 - 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-proBNP 1-76 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.
AB - 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-proBNP 1-76 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.
KW - ANP
KW - BNP
KW - NT-proBNP
KW - hypertension
KW - natriuretic peptide
KW - proBNP
UR - http://www.scopus.com/inward/record.url?scp=84867385312&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84867385312&partnerID=8YFLogxK
U2 - 10.1016/j.jacc.2012.05.049
DO - 10.1016/j.jacc.2012.05.049
M3 - Article
C2 - 23058313
AN - SCOPUS:84867385312
SN - 0735-1097
VL - 60
SP - 1558
EP - 1565
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 16
ER -