Brain natriuretic peptide (1-32) (human)

Brain natriuretic peptide is a cardiac neurohormone that is secreted by the left ventricle in response to an increase in wall stress ^[2]. BNP has emerged as an important cardiac neuro-hormone with multiple potential roles in the management of patients with cardiac dysfunction, Brain natriuretic peptide (1-32) (human) is the active part of BNP ^[3,4].

Brain natriuretic peptide (1-32) (human) regulates the production of major inflammatory molecules, such as reactive oxygen- and nitrogen species (ROS and RNS), leukotriene B(4) (LTB(4)), prostaglandin E(2) (PGE(2)); modulates the cytokines (TNF-alpha, IL-12 and IL-10) profile, and affects cell motility^[1].

In a consecutive series of 200 patients referred for echocardiographic assessment of LV function , those with normal function had substantially lower Brain natriuretic peptide (1-32) (human) levels than those with LV (systolic, diastolic or combined) dysfunction. In this population with a very high prevalence of LV dysfunction (47.5%), a Brain natriuretic peptide (1-32) (human) of 75 pg/ml or more was highly accurate at identifying such patients. In this highly selected group, BNP-32 testing appears to be a very good screening tool^[5].

When evaluated the utility of Brain natriuretic peptide (1-32) (human)-guided ACE inhibitor titration compared with clinically guided titration in a small randomized trial. Comprehensive hemodynamic assessment was performed at the study onset and after 8 weeks of treatment. At study end, the ACE inhibitor dose was significantly greater (p = 0.006) and heart rate was significantly reduced (p = 0.02) in the BNP-32 group compared with the clinically guided group^[6].

The utility of Brain natriuretic peptide (1-32) (human) testing to screen for systolic or diastolic dysfunction was evaluated in a substudy of the Heart and Soul study. In this group of stable out-patients with known coronary disease, an elevated BNP-32 level (>100 pg/ml) was associated with both systolic and diastolic dysfunction^[7].

References:
[1]. Chiurchiù V, Izzi V, et,al. Brain Natriuretic Peptide (BNP) regulates the production of inflammatory mediators in human THP-1 macrophages. Regul Pept. 2008 Jun 5;148(1-3):26-32. doi: 10.1016/j.regpep.2008.02.009. Epub 2008 Mar 10. PMID: 18410972.
[2]. Wasywich CA, Whalley GA, et,al. Brain natriuretic peptide in the contemporary management of congestive heart failure. Expert Rev Cardiovasc Ther. 2005 Jan;3(1):71-84. doi: 10.1586/14779072.3.1.71. PMID: 15723576.
[3]. Sudoh T, Maekawa K, et,al. Cloning and sequence analysis of cDNA encoding a precursor for human brain natriuretic peptide. Biochem Biophys Res Commun. 1989 Mar 31;159(3):1427-34. doi: 10.1016/0006-291x(89)92269-9. PMID: 2522777.
[4]. Hunt PJ, Yandle TG, et,al. The amino-terminal portion of pro-brain natriuretic peptide (Pro-BNP) circulates in human plasma. Biochem Biophys Res Commun. 1995 Sep 25;214(3):1175-83. doi: 10.1006/bbrc.1995.2410. PMID: 7575527.
[5]. Maisel AS, Koon J, et,al. Utility of B-natriuretic peptide as a rapid, point-of-care test for screening patients undergoing echocardiography to determine left ventricular dysfunction. Am Heart J. 2001 Mar;141(3):367-74. doi: 10.1067/mhj.2001.113215. PMID: 11231433.
[6]. Murdoch DR, McDonagh TA, et,al. Titration of vasodilator therapy in chronic heart failure according to plasma brain natriuretic peptide concentration: randomized comparison of the hemodynamic and neuroendocrine effects of tailored versus empirical therapy. Am Heart J. 1999 Dec;138(6 Pt 1):1126-32. doi: 10.1016/s0002-8703(99)70079-7. PMID: 10577444.
[7]. Bibbins-Domingo K, Ansari M, et,al. Is B-type natriuretic peptide a useful screening test for systolic or diastolic dysfunction in patients with coronary disease? Data from the Heart and Soul Study. Am J Med. 2004 Apr 15;116(8):509-16. doi: 10.1016/j.amjmed.2003.08.037. PMID: 15063811; PMCID: PMC2776680.

脑利钠肽是一种心脏神经激素,由左心室响应壁应力增加而分泌^[2]。 BNP 已成为一种重要的心脏神经激素,在心功能不全患者的管理中具有多种潜在作用,脑利钠肽 (1-32)（人）是 BNP 的活性部分 ^[3,4].

脑利钠肽 (1-32)（人类）调节主要炎症分子的产生,例如活性氧和氮类（ROS 和 RNS）、白三烯 B(4) (LTB(4))、前列腺素 E (2) (铂族元素(2));调节细胞因子（TNF-α、IL-12 和 IL-10）分布,并影响细胞运动^[1]。

在连续 200 名接受超声心动图评估 LV 功能的患者中,功能正常的患者的脑利钠肽 (1-32)（人类）水平明显低于 LV（收缩、舒张或联合）功能障碍的患者。在这个 LV 功能障碍患病率非常高 (47.5%) 的人群中,75 pg/ml 或更高的脑利钠肽 (1-32)（人类）在识别此类患者时非常准确。在这个经过高度筛选的群体中,BNP-32 测试似乎是一种非常好的筛选工具^[5]。

在一项小型随机试验中评估脑利钠肽 (1-32)（人）指导的 ACE 抑制剂滴定与临床指导滴定的效用。在研究开始时和治疗 8 周后进行全面的血液动力学评估。在研究结束时,与临床指导组相比,BNP-32 组的 ACE 抑制剂剂量显着增加 (p = 0.006),心率显着降低 (p = 0.02)^[6]。

心与灵魂研究的一项子研究评估了脑利钠肽 (1-32)（人类）测试在筛查收缩或舒张功能障碍方面的效用。在这组患有已知冠心病的稳定门诊患者中,升高的 BNP-32 水平 (>100 pg/ml) 与收缩和舒张功能障碍相关^[7]。