Department of Medicine, Weill Cornell Medical College, New York Presbyterian Hospital, New York, New York 10065, USA.
J Am Coll Cardiol. 2012 Oct 16;60(16):1558-65. doi: 10.1016/j.jacc.2012.05.049.
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.
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.
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.
Compared to normotensive, BNP(1-32) and N-terminal proBNP(1-76) (NT-proBNP(1-76)) were significantly decreased in pre-hypertension (p < 0.05), with BNP(1-32) significantly decreased in stage 1 as well (p < 0.05). Although proBNP(1-108) remained unchanged, the processed form was significantly increased only in stage 2 hypertension (p < 0.05). ANP(1-28) remained unchanged, while NT-ANP(1-98) was reduced in pre-hypertension (p < 0.05).
The authors demonstrated the existence of an impaired production and/or release of proBNP(1-108) along with a concomitant reduction of BNP(1-32) 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.
本研究旨在探讨循环心钠肽、心房钠尿肽(ANP)和 B 型或脑钠尿肽(BNP)在普通人群中的血浆水平,重点研究其在人类高血压恶化中的相对差异。
尽管 ANP 和 BNP 是人体血压的特征性调节因子,但在人群水平上,它们与高血压的关系知之甚少。作者假设高血压与这些激素或其分子前体的激活不足有关。
研究队列(N=2082,年龄>45 岁)来自明尼苏达州罗彻斯特的随机样本,每位患者均有病史、临床检查和不同形式的 ANP 和 BNP 血浆评估。患者根据血压分层。多变量线性回归用于评估高血压恶化时利钠肽水平的差异。
与正常血压相比,高血压前期患者 BNP(1-32)和 N 末端 proBNP(1-76)(NT-proBNP(1-76))明显降低(p<0.05),1 期高血压患者 BNP(1-32)也明显降低(p<0.05)。虽然 proBNP(1-108)保持不变,但仅在 2 期高血压时处理形式显著增加(p<0.05)。ANP(1-28)保持不变,而 NT-ANP(1-98)在高血压前期降低(p<0.05)。
作者证明了在高血压早期存在 proBNP(1-108)的产生和/或释放受损,以及 BNP(1-32)和 NT-proBNP(1-76)的同时降低,仅在 2 期高血压时显著升高。重要的是,他们同时证明了在晚期高血压中缺乏代偿性 ANP 升高。