Author/Authors :
Macheret، نويسنده , , Fima and Heublein، نويسنده , , Denise and Costello-Boerrigter، نويسنده , , Lisa C. Costello-Boerrigter، نويسنده , , Guido and McKie، نويسنده , , Paul and Bellavia، نويسنده , , Diego and Mangiafico، نويسنده , , Sarah and Ikeda، نويسنده , , Yasuhiro and Bailey، نويسنده , , Kent and Scott، نويسنده , , Christopher G. and Sandberg، نويسنده , , Sharon and Chen، نويسنده , , Horng H. and Malatino، نويسنده , , Lorenzo and Redfield، نويسنده , , Margaret M. and Rodeheffer، نويسنده , , Richard and Burnett Jr، نويسنده , , John and Cataliotti، نويسنده , , Alessandro، نويسنده ,
Abstract :
Objectives
tudy 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.
ound
gh 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.
s
udy 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.
s
ed 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).
sions
thors 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.
Keywords :
BNP , hypertension , proBNP , ANP , NT-proBNP , Natriuretic peptide