Brain natriuretic peptide (1-32) (human)
(Synonyms: 奈西立肽; Brain Natriuretic Peptide-32 human; BNP-32) 目录号 : GC17895
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。
Cas No.:124584-08-3
Sample solution is provided at 25 µL, 10mM.
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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]。
| Cas No. | 124584-08-3 | SDF | |
| 别名 | 奈西立肽; Brain Natriuretic Peptide-32 human; BNP-32 | ||
| 化学名 | (1E,3S,4Z,6S,7Z,9S,10Z,12S,13Z,15S,16Z,18S)-18-((1H-imidazol-5-yl)methyl)-1-((4R,5E,8Z,10S,11Z,14Z,16S,17Z,19S,20Z,22S,23E,25S,26Z,28S,29Z,31S,32E,34S,35Z,37S,38E,40S,41Z,43S,44Z,47Z,49S,50Z,52R)-52-((Z)-((1Z,3S,4Z,6S,7Z,9S,10Z,12S,13Z,16Z,18S,19Z)-1-((S) | ||
| Canonical SMILES | CC[C@]([C@@]1([H])/C(O)=N/[C@@](/C(O)=N\[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/C/C(O)=N/[C@@](/C(O)=N/C/C(O)=N\[C@@](/C(O)=N\[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](C(O)=O)([H])CC2=CN=CN2)([H])CCCNC(N)=N)([H])CCCNC(N | ||
| 分子式 | C143H244N50O42S4 | 分子量 | 3464.05 |
| 溶解度 | Soluble to 24mg/ml in sterile water | 储存条件 | -20°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.2887 mL | 1.4434 mL | 2.8868 mL |
| 5 mM | 0.0577 mL | 0.2887 mL | 0.5774 mL |
| 10 mM | 0.0289 mL | 0.1443 mL | 0.2887 mL |
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The Utility of Brain Natriuretic Peptide in Pediatric Cardiology: A Review
Pediatr Crit Care Med2016 Nov;17(11):e529-e538.PMID: 27749513DOI: 10.1097/PCC.0000000000000966
Objective: The aim of this article is to evaluate the clinical utility of brain natriuretic peptide in pediatric patients, examining the diagnostic value, management, and prognostic relevance, by critical assessment of the literature. Data sources: In December 2015, a literature search was performed (PubMed access to MEDLINE citations; http://www.ncbi.nlm.nih.gov/PubMed/) and included these Medical Subject Headings and text terms for the key words: "brain natriuretic peptide," "amino-terminal pro-brain natriuretic peptide," "children," "neonate/s," "newborn/s," "infant/s," and "echocardiography." Study selection: Each article title and abstract was screened to identify relevant studies. The search strategy was limited to published studies in English language concerning brain natriuretic peptide/amino-terminal pro-brain natriuretic peptide in pediatric patients. Data extraction: Data on age, gender, type of clinical condition, brain natriuretic peptide assay method, cardiac function variables evaluated by echocardiography, and prognosis were extracted. Data synthesis: Brain natriuretic peptide reference values in healthy newborns, infants, and children are presented. Brain natriuretic peptide diagnostic accuracy in newborns, infants, and children suspected to have congenital heart defects is discussed, and brain natriuretic peptide prognostic value reviewed. The data suggest that the determination of brain natriuretic peptide levels improves the diagnostic accuracy in the assessment of heart disease in the pediatric population. Brain natriuretic peptide assay may increase the accuracy of neonatal screening programs for diagnosing congenital heart defects. Echocardiographic variables correlated to brain natriuretic peptide levels. Additionally, brain natriuretic peptide levels predicted adverse outcomes in the postoperative period. Conclusions: Brain natriuretic peptide assessment is a reliable test to diagnose significant structural or functional cardiovascular disease in children. In the integrated follow-up of these cases, several physiologic and clinical variables must be considered; brain natriuretic peptide may be an additional helpful marker. Nevertheless, larger prospective studies are warranted to elucidate the true prognostic value of brain natriuretic peptide in pediatric patients.
Brain natriuretic peptide: a biomarker for all cardiac disease?
Curr Opin Cardiol2014 Mar;29(2):160-6.PMID: 24406448DOI: 10.1097/HCO.0000000000000036
Purpose of review: To evaluate new development in the utility of brain natriuretic peptide and N-Terminal brain natriuretic peptide (BNP/NT-Pro-BNP) in the management of various cardiovascular diseases. The determination of plasma BNP levels has an established role in the discrimination of pulmonary oedema from other causes of acute dyspnoea, and there is increasing evidence of the utility of BNP/NT-Pro-BNP assay both as a prognostic tool in chronic heart failure and as a means of guiding therapy in heart failure patients aged below 70 years.
Recent findings: Findings have substantially extended the clinical utility of BNP/NT-Pro-BNP assay. In heart failure with preserved left ventricular ejection fraction, BNP elevation may also facilitate diagnosis, although its precise utility is uncertain.In the acute catecholamine-induced myocardial inflammatory condition of Tako-Tsubo cardiomyopathy (TTC), BNP/NT-Pro-BNP elevations are marked and persist for at least 3 months, despite the absence of pulmonary oedema. In TTC, BNP/NT-Pro-BNP therefore serves as an ancillary diagnostic measure as well as a marker of recovery. Among other conditions in which BNP assay may provide prognostic information are atrial fibrillation (in which the extent of elevation predicts thromboembolic risk) and pulmonary hypertension.
Summary: BNP/NT-Pro-BNP assay has widespread utility as an adjunct to cardiovascular disease diagnosis and management.
Brain Natriuretic Peptide: It's Not About the Brain or Just Another Smart Polypeptide--It's About the Heart
Neonatal Netw2015;34(6):355-9.PMID: 26803017DOI: 10.1891/0730-0832.34.6.355
Brain natriuretic peptide (BNP) is a cardiac hormone with diuretic, natriuretic, and vasodilator properties. Measurement of plasma B-type natriuretic peptide concentrations is increasingly used to aid diagnosis, assess prognosis, and tailor treatment in adults with congestive heart failure. Recent studies suggest that the peptide is also useful in pediatric patients. The diagnostic role of plasma BNP in neonates admitted to the NICU has shown promise as an aid in diagnosis in neonates with signs of congenital heart disease; as a biomarker of bronchopulmonary dysplasia, patent ductus arteriosus, and persistent pulmonary hypertension of the newborn; a predictive biomarker of the response to indomethacin in preterm infants; and, more significantly, in acute heart failure.
Brain natriuretic peptide: role in cardiovascular and volume homeostasis
Semin Nephrol2002 Sep;22(5):423-37.PMID: 12224050DOI: 10.1053/snep.2002.35666
The identification of natriuretic peptides as key regulators of natriuresis and vasodilatation, and the appreciation that their secretion is under the control of cardiac hemodynamic and neurohumoral factors, has caused wide interest. The natriuretic peptides are structurally similar, but genetically distinct peptides that have diverse actions on cardiovascular, renal, and endocrine homeostasis. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are of myocardial cell origin, while cardiac natriuretic peptide (CNP) is of endothelial origin. ANP and BNP bind to the natriuretic peptide receptor (NPR-A) which, via 3' 5'-cyclic guanosine monophosphate (cGMP), mediates natriuresis, vasodialation, renin inhibition, and antimitogenic properties. CNP lacks natriuretic action but possesses vasodilating and growth inhibiting effects via the guanyl cyclase linked natriuretic peptide-B (NPR-B) receptor. All three peptides are cleared by natriuretic peptide-C receptor (NPR-C) and degraded by neutral endopeptidase, both of which are widely expressed in kidney, lung, and vascular wall. Recently, a fourth member of the natriuretic peptide, dendroaspsis natriuretic peptide (DNP) has been reported to be present in human plasma and atrial myocardium.
NT-ProBNP: the mechanism behind the marker
J Card Fail2005 Jun;11(5 Suppl):S81-3.PMID: 15948107DOI: 10.1016/j.cardfail.2005.04.019
Brain natriuretic peptide (BNP) was isolated originally from porcine brain extracts but was soon defined as a cardiac natriuretic hormone. Together with the highly homologous atrial natriuretic peptide, it forms a dual natriuretic peptide system of the heart. The main stimulus for proBNP synthesis and secretion from cardiac myocytes is myocyte stretch. On secretion, the propeptide is split into the biologically active BNP and the remaining part of the prohormone N-terminal proBNP (NT-proBNP). In heart failure increased wall stretch, neurohormonal activation and hypoxia stimulate BNP secretion. The recently demonstrated production of BNP by stimulated cardiac fibroblasts is of uncertain pathophysiologic importance. In contrast to atrial natriuretic peptide, BNP is a constitutively secreted hormone with relatively little intracellular storage of mature peptide. In the normal state, the atrium is the main cardiac production site, but as heart failure develops, there is a profound activation of ventricular NT-proBNP synthesis. BNP acts on distant tissues and causes diuresis, vasodilatation, and decreased renin and aldosterone secretion. Known mechanisms of BNP clearance from plasma include binding to the natriuretic peptide clearance receptor type-C and proteolysis by peptidase NEP 24.11. NT-proBNP has a longer half-life and thus higher plasma concentration than BNP. It probably is cleared from plasma by renal excretion and possibly other unknown pathways.