WordNet

kill by smashing someones skull
mental ability; "hes got plenty of brains but no common sense" (同)brainpower, learning_ability, mental capacity, mentality, wit
that part of the central nervous system that includes all the higher nervous centers; enclosed within the skull; continuous with the spinal cord (同)encephalon
the brain of certain animals used as meat
hit on the head
amide combining the amino group of one amino acid with the carboxyl group of another; usually obtained by partial hydrolysis of protein
of or relating to natriuresis

PrepTutorEJDIC

『脳』,脳髄 / 《しばしば複数形で》『頭脳』,『知力』 / 《話》秀才,知的指導者 / …‘の'頭を打ち砕く
=brassiere,　brassiere

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/03 10:45:31」(JST)

wiki en

Basic natriuretic peptide (BNP), now known as B-type natriuretic peptide (also BNP) or GC-B, is a 32 amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes). The release of BNP is modulated by calcium ions. ^[1] BNP is named as such because it was originally identified in extracts of porcine brain, although in humans it is produced mainly in the cardiac ventricles.

BNP is secreted along with a 76 amino acid N-terminal fragment (NT-proBNP) which is biologically inactive. BNP binds to and activates the atrial natriuretic factor receptors NPRA, and to a lesser extent NPRB, in a fashion similar to atrial natriuretic peptide (ANP) but with 10-fold lower affinity. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better targets than ANP for diagnostic blood testing.

The physiologic actions of BNP are similar to ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. Thus, the net effect of BNP and ANP is a decrease in blood volume which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction.

Diagnostic significance

The main clinical utility of either BNP or NT-BNP is that a normal level rules out acute heart failure in the emergency setting. ^[2]
Either marker can also be used for screening and prognosis of heart failure.^[3]
Both are also typically increased in patients with left ventricular dysfunction, with or without symptoms (BNP accurately reflects current ventricular status, as its half-life is 20 minutes, as opposed to 1–2 hours for NT-ProBNP).^[4]

BNP less than 100 pg per milliliter

sensitivity = 90%
specificity = 76%

BNP less than 50 pg per milliliter

sensitivity = 97%
specificity = 62%

some laboratories report in units ng per Litre (ng/L) which is equivalent to pg/ml
For patients with congestive heart failure, BNP values will generally be above 100 pg/ml.
A more conservative interpretation of the BNP is that normal values are less than 50 pg/ml, in order to achieve adequate sensitivity.
There is a diagnostic 'gray area', often defined as between 100 and 500 pg/ml, for which the test is considered inconclusive, but levels above 500 pg/ml are generally considered to be positive. This so called gray zone has been addressed in several studies and using clinical history or other available simple tools can help make the diagnosis.^[5]^[6]

Bhalla et al. showed that BNP plays a very important role in prognostication of millions of diabetics.^[7]
Also, BNP was found to have an important role in prognostication of heart surgery patients^[8] and in the emergency department.^[9] Bhalla et al. showed that combining BNP with other tools like ICG can improve early diagnosis of heart failure and advance prevention strategies.^[10]^[11] Utility of BNP has also been explored in various settings like preeclampsia, ICU and shock and ESRD.^[12]^[13]^[14]

The effect or race and gender on value of BNP and its utility in that context has been studied extensively.^[15]^[16]

NT-proBNP levels (in pg/mL) by NYHA functional class ^[17]
	NYHA I	NYHA II	NYHA III	NYHA IV
5th Percentile	33	103	126	148
Mean	1015	1666	3029	3465
95th Percentile	3410	6567	10,449	12,188

BNP can be elevated in renal failure^{[citation needed]} BNP is cleared by binding to natriuretic peptide receptors (NPRs) and neutral endopeptidase (NEP) Less than 5% of BNP is cleared renally. NTproBNP is the inactive molecule resulting from cleavage of the prohormone Pro-BNP and is SOLELY reliant on the kidney for excretion. The achilles heel of the NT proBNP molecule is the overlap in kidney disease in the heart failure patient population.^[18]^[19]

Usual ranges for brain natriuretic peptide (BNP)
Patient type		Lower limit	Upper limit	Unit
Male	45-54 yrs	4^[20]	40^[20]	pg/mL
	55-64 yrs	5^[20]	52^[20]
	65-74 yrs	7^[20]	67^[20]
	75-83 yrs	9^[20]	86^[20]
Female	45-54 yrs	8^[20]	73^[20]
	55-64 yrs	10^[20]	93^[20]
	65-74 yrs	13^[20]	120^[20]
	75-83 yrs	16^[20]	155^[20]

The BNP test is used as an aid in the diagnosis and assessment of severity of congestive heart failure (also referred to as heart failure). A recent meta-analysis concerning effects of BNP testing on clinical outcomes of patients presenting to the emergency department with acute dyspnea revealed that BNP testing led to a decrease in admission rates and decrease in mean length of stay, although neither were statistically significant. Effects on all cause hospital mortality was inconclusive.^[21] The BNP test is also used for the risk stratification of patients with acute coronary syndromes.^[22]^[23]

When interpreting an elevated BNP level, it is useful to remember that values may be elevated due to factors other than heart failure. Lower levels are often seen in obese patients.^[24] Higher levels are seen in those with renal disease, in the absence of heart failure.

BNP is also one of the reasons why people will feel the need to urinate after getting into the bathtub or pool. The increased pressure on the body drives more fluid back into systemic circulation which in turn leads to a slight increase in preload. The left ventricle, and to a small degree the left atrium, secrete BNP in response. The natriuretic effect of BNP leads to an increase in urine production.^[25]

Clinical significance

Recombinant BNP, Nesiritide is used to treat decompensated heart failure. However, a recent clinical trial^[26] failed to show a benefit of nesiritide in patients with acute decompensated heart failure and the authors could not recommend its use.

Measurement and standardization

BNP and NT-proBNP are measured by immunoassay. BNP is standardised whereas NT-proBNP has not been standardised yet.

References

^ Ziskoven D, Forssmann WG, Holthausen U, Menz G, Addicks K, Rippegater G: Calcium Calmodulinantagonists Influences the release of Cardiodilatin/ANP from Atrial Cardiocytes. Handbook Endocrinology of the Heart, edited by Kaufmann W, Wambach G, 01/1989; Springer Verlag Berlin Heidelberg New York; ISBN/EAN 978-3-540-51409-1
^ Maisel A, Krishnaswamy P, Nowak R, McCord J, Hollander J, Duc P, Omland T, Storrow A, Abraham W, Wu A, Clopton P, Steg P, Westheim A, Knudsen C, Perez A, Kazanegra R, Herrmann H, McCullough P (2002). "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure". N Engl J Med 347 (3): 161–7. doi:10.1056/NEJMoa020233. PMID 12124404.
^ Bhalla V, Willis S, Maisel AS (2004). "B-type natriuretic peptide: the level and the drug--partners in the diagnosis of congestive heart failure". Congest Heart Fail 10 (1 Suppl 1): 3–27. doi:10.1111/j.1527-5299.2004.03310.x. PMID 14872150.
^ Atisha D, Bhalla MA, Morrison LK, Felicio L, Clopton P, Gardetto N, Kazanegra R, Chiu A, Maisel AS (September 2004). "A prospective study in search of an optimal B-natriuretic peptide level to screen patients for cardiac dysfunction". Am. Heart J. 148 (3): 518–23. doi:10.1016/j.ahj.2004.03.014. PMID 15389242.
^ Strunk A, Bhalla V, Clopton P, Nowak RM, McCord J, Hollander JE, Duc P, Storrow AB, Abraham WT, Wu AH, Steg G, Perez A, Kazanegra R, Herrmann HC, Aumont MC, McCullough PA, Maisel A (January 2006). "Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the Breathing Not Properly Multinational Study". Am. J. Med. 119 (1): 69.e1–11. doi:10.1016/j.amjmed.2005.04.029. PMID 16431187.
^ Brenden CK, Hollander JE, Guss D, McCullough PA, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Bhalla V, Clopton P, Jesse R, Maisel AS (May 2006). "Gray zone BNP levels in heart failure patients in the emergency department: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study". Am. Heart J. 151 (5): 1006–11. doi:10.1016/j.ahj.2005.10.017. PMID 16644322.
^ Bhalla MA, Chiang A, Epshteyn VA, Kazanegra R, Bhalla V, Clopton P, Krishnaswamy P, Morrison LK, Chiu A, Gardetto N, Mudaliar S, Edelman SV, Henry RR, Maisel AS (September 2004). "Prognostic role of B-type natriuretic peptide levels in patients with type 2 diabetes mellitus". J. Am. Coll. Cardiol. 44 (5): 1047–52. doi:10.1016/j.jacc.2004.05.071. PMID 15337217.
^ Hutfless R, Kazanegra R, Madani M, Bhalla MA, Tulua-Tata A, Chen A, Clopton P, James C, Chiu A, Maisel AS (May 2004). "Utility of B-type natriuretic peptide in predicting postoperative complications and outcomes in patients undergoing heart surgery". J. Am. Coll. Cardiol. 43 (10): 1873–9. doi:10.1016/j.jacc.2003.12.048. PMID 15145114.
^ Maisel A, Hollander JE, Guss D, McCullough P, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Bhalla V, Clopton P, Jesse R (September 2004). "Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT). A multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath". J. Am. Coll. Cardiol. 44 (6): 1328–33. doi:10.1016/j.jacc.2004.06.015. PMID 15364340.
^ Bhalla V, Isakson S, Bhalla MA, Lin JP, Clopton P, Gardetto N, Maisel AS (February 2005). "Diagnostic ability of B-type natriuretic peptide and impedance cardiography: testing to identify left ventricular dysfunction in hypertensive patients". Am. J. Hypertens. 18 (2 Pt 2): 73S–81S. doi:10.1016/j.amjhyper.2004.11.044. PMID 15752936.
^ Castellanos LR, Bhalla V, Isakson S, Daniels LB, Bhalla MA, Lin JP, Clopton P, Gardetto N, Hoshino M, Chiu A, Fitzgerald R, Maisel AS (February 2009). "B-type natriuretic peptide and impedance cardiography at the time of routine echocardiography predict subsequent heart failure events". J. Card. Fail. 15 (1): 41–7. doi:10.1016/j.cardfail.2008.09.003. PMID 19181293.
^ Resnik JL, Hong C, Resnik R, Kazanegra R, Beede J, Bhalla V, Maisel A (August 2005). "Evaluation of B-type natriuretic peptide (BNP) levels in normal and preeclamptic women". Am. J. Obstet. Gynecol. 193 (2): 450–4. doi:10.1016/j.ajog.2004.12.006. PMID 16098869.
^ Bhalla V, Bhalla MA, Maisel AS (August 2004). "Evolution of B-type natriuretic peptide in evaluation of intensive care unit shock". Crit. Care Med. 32 (8): 1787–9. doi:10.1097/01.CCM.0000135748.75590.54. PMID 15286561.
^ Sheen V, Bhalla V, Tulua-Tata A, Bhalla MA, Weiss D, Chiu A, Abdeen O, Mullaney S, Maisel A (February 2007). "The use of B-type natriuretic peptide to assess volume status in patients with end-stage renal disease". Am. Heart J. 153 (2): 244.e1–5. doi:10.1016/j.ahj.2006.10.041. PMID 17239684.
^ Maisel AS, Clopton P, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, Omland T, Storrow AB, Abraham WT, Wu AH, Steg G, Westheim A, Knudsen CW, Perez A, Kazanegra R, Bhalla V, Herrmann HC, Aumont MC, McCullough PA (June 2004). "Impact of age, race, and sex on the ability of B-type natriuretic peptide to aid in the emergency diagnosis of heart failure: results from the Breathing Not Properly (BNP) multinational study". Am. Heart J. 147 (6): 1078–84. doi:10.1016/j.ahj.2004.01.013. PMID 15199359.
^ Daniels LB, Bhalla V, Clopton P, Hollander JE, Guss D, McCullough PA, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Jesse R, Maisel A (May 2006). "B-type natriuretic peptide (BNP) levels and ethnic disparities in perceived severity of heart failure: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study of BNP levels and emergency department decision making in patients presenting with shortness of breath". J. Card. Fail. 12 (4): 281–5. doi:10.1016/j.cardfail.2006.01.008. PMID 16679261.
^ "N-terminal pro-BNP".
^ Austin WJ, Bhalla V, Hernandez-Arce I, Isakson SR, Beede J, Clopton P, Maisel AS, Fitzgerald RL (October 2006). "Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease". Am. J. Clin. Pathol. 126 (4): 506–12. doi:10.1309/M7AAXA0J1THMNCDF. PMID 16938661.
^ Daniels, LB; Clopton, P; Bhalla, V; Krishnaswamy, P; Nowak, RM; McCord, J; Hollander, JE; Duc, P et al. (May 2006). "Results from the Breathing Not Properly Multinational Study". Am. Heart J. 151 (5): 999–1005. doi:10.1016/j.ahj.2005.10.011. PMID 16644321.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p Saint Francis Hospital Laboratory > BNP reference range change Jay Hupp & Dr. Michel S. Medawar. Effective November, 2002
^ Lam, LL; Cameron, PA; Schneider, HG; Abramson, MJ; Müller, C; Krum, H (2010). "Meta-analysis: effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting". Annals of internal medicine 153 (11): 728–35. doi:10.1059/0003-4819-153-11-201012070-00006. PMID 21135296.
^ Bibbins-Domingo K, Gupta R, Na B, Wu AH, Schiller NB, Whooley MA (January 2007). "N-terminal fragment of the prohormone brain-type natriuretic peptide (NT-proBNP), cardiovascular events, and mortality in patients with stable coronary heart disease". JAMA 297 (2): 169–76. doi:10.1001/jama.297.2.169. PMC 2848442. PMID 17213400.
^ Fitzgerald RL, Cremo R, Gardetto N, Chiu A, Clopton P, Bhalla V, Maisel AS (September 2005). "Effect of nesiritide in combination with standard therapy on serum concentrations of natriuretic peptides in patients admitted for decompensated congestive heart failure". Am. Heart J. 150 (3): 471–7. doi:10.1016/j.ahj.2004.11.021. PMID 16169326.
^ Wang TJ, Larson MG, Levy D, et al. (2004). "Impact of obesity on plasma natriuretic peptide levels". Circulation. 109 (5): 594–600. doi:10.1161/01.CIR.0000112582.16683.EA. PMID 14769680.
^ Diagnostic Pearls in Cardiorespiratory Disease. CVMA Yosemite Conference 2010. Bruce Keene, DVM, MSc, DACVIM (Cardiology)
^ O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. The New England journal of medicine 2011;365:32-43.

External links

Brain Natriuretic Peptide at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

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1. 心不全におけるナトリウム利尿ペプチド測定 natriuretic peptide measurement in heart failure
2. 非心不全下におけるナトリウム利尿ペプチド測定 natriuretic peptide measurement in non heart failure settings
3. 心血管疾患の危険因子の概要 overview of the possible risk factors for cardiovascular disease
4. 乳幼児および小児における心不全の病因および診断 etiology and diagnosis of heart failure in infants and children
5. ST上昇型心筋梗塞後の有害転帰の危険因子 risk factors for adverse outcomes after st elevation myocardial infarction

English Journal

Depressive symptoms in outpatients with heart failure: Importance of inflammatory biomarkers, disease severity and personality.

Brouwers C1, Kupper N, Pelle AJ, Szabó BM, Westerhuis BL, Denollet J.Author information 1a Department of Medical Psychology and Clinical Psychology, CoRPS-Center of Center of Research on Psychology in Somatic Diseases , Tilburg University , Tilburg , The Netherlands.AbstractObjective: Depressive symptoms are highly prevalent in heart failure (HF) patients, however the underlying etiology of depression in HF patients remains yet unclear. Hence, the goal is to examine the relative importance of inflammation, disease severity and personality as predictors of depression in HF patients. Design: Depressive symptoms (Hospital Anxiety and Depression Scale, depression subscale) were assessed at baseline and one-year follow-up in 268 HF patients (75.6% men; mean age = 66.7 ± 8.7). Markers of inflammation (TNFα, sTNFr1, sTNFr2, IL-6 and IL-10), disease severity (e.g. New York Heart Association (NYHA) classification) and personality (Type D personality, loneliness) were assessed at baseline. Results: At baseline, NYHA class, body mass index, educational level, Type D personality and loneliness were significantly associated with depression. Higher NYHA class (B = 2.25; SE = .83), higher educational level (B = 1.41; SE = .48), Type D personality (B = 2.56; SE = .60) and loneliness (B = .19; SE = .05) were also independently associated with higher depression levels at one-year follow-up (all p-values < .005). Inflammation, brain natriuretic peptide and left ventricular ejection fraction were not related to depression over time. Conclusions: Personality factors, but not inflammation, were independent concomitants of depressive symptoms in patients with HF. Gaining more insight into the etiology of depression in HF patients is important in order to identify potential targets for novel interventions.
Psychology & health.Psychol Health.2014 May;29(5):564-82. doi: 10.1080/08870446.2013.869813. Epub 2014 Jan 3.
Objective: Depressive symptoms are highly prevalent in heart failure (HF) patients, however the underlying etiology of depression in HF patients remains yet unclear. Hence, the goal is to examine the relative importance of inflammation, disease severity and personality as predictors of depression in
PMID 24286171

Acute mercury toxicity modulates cytochrome P450, soluble epoxide hydrolase and their associated arachidonic acid metabolites in C57Bl/6 mouse heart.

Amara IE1, Elshenawy OH1, Abdelrady M1, El-Kadi AO2.Author information 1Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, T6G 2E1, AB, Canada.2Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, T6G 2E1, AB, Canada; College of Pharmacy, Qatar University, Doha, Qatar. Electronic address: aelkadi@ualberta.ca.AbstractMercury exposure is associated with increased risk of cardiovascular disease and profound cardiotoxicity. However, the correlation between Hg(2+)-mediated toxicity and alteration in cardiac cytochrome P450s (Cyp) and their dependent arachidonic acid metabolites has never been investigated. Therefore, we investigated the effect of acute mercury toxicity on the expression of Cyp-epoxygenases and Cyp-ω-hydroxylases and their associated arachidonic acid metabolites in mice hearts. In addition, we examined the expression and activity of soluble epoxide hydrolase (sEH) as a key player in arachidonic acid metabolism pathway. Mercury toxicity was induced by a single intraperitoneal injection (IP) of 2.5mg/kg of mercuric chloride (HgCl2). Our results showed that mercury treatment caused a significant induction of the cardiac hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP); in addition to Cyp1a1, Cyp1b1, Cyp2b9, Cyp2b10, Cyp2b19, Cyp2c29, Cyp2c38, Cyp4a10, Cyp4a12, Cyp4a14, Cyp4f13, Cyp4f15, Cyp4f16 and Cyp4f18 gene expression. Moreover, Hg(2+) significantly increased sEH protein expression and activity levels in hearts of mercury-treated mice, with a consequent decrease in 14,15-, and 11,12-epoxyeicosatrienoic acids (EETs) levels. Whereas the formation of 14,15-, 11,12-, 8,9-dihydroxyeicosatrienoic acids (DHETs) was significantly increased. In conclusion, acute Hg(2+) toxicity modulates the expression of several Cyp and sEH enzymes with a consequent decrease in the cardioprotective EETs which could represent a novel mechanism by which mercury causes progressive cardiotoxicity. Furthermore, inhibiting sEH might represent a novel therapeutic approach to prevent Hg(2+)-induced hypertrophy.
Toxicology letters.Toxicol Lett.2014 Apr 7;226(1):53-62. doi: 10.1016/j.toxlet.2014.01.025. Epub 2014 Jan 25.
Mercury exposure is associated with increased risk of cardiovascular disease and profound cardiotoxicity. However, the correlation between Hg(2+)-mediated toxicity and alteration in cardiac cytochrome P450s (Cyp) and their dependent arachidonic acid metabolites has never been investigated. Therefore
PMID 24472606

Berberine improves pressure overload-induced cardiac hypertrophy and dysfunction through enhanced autophagy.

Li MH1, Zhang YJ1, Yu YH1, Yang SH1, Iqbal J2, Mi QY3, Li B1, Wang ZM1, Mao WX1, Xie HG4, Chen SL5.Author information 1Division of Cardiovascular Medicine, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, China.2Department of Cardiovascular Science, University of Sheffield, UK.3Central Laboratory, General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.4Central Laboratory, General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, China; Department of Pharmacology, Nanjing Medical University School of Pharmacy, Nanjing, China.5Division of Cardiovascular Medicine, Department of Medicine, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, China. Electronic address: chmengx126@gmail.com.AbstractCardiac hypertrophy is a maladaptive change in response to pressure overload, and is also an important risk for developing heart failure. Berberine is known to have cardioprotective effects in patients with hypertension and in animal models of cardiac hypertrophy. In the current study, we observed that transverse aortic contraction (TAC) surgery induced a marked increase in heart size, the ratio of heart weight to body weight, cardiomyocyte apoptosis, myocardial fibrosis, and hypertrophic marker brain natriuretic peptide, all of which were effectively suppressed by berberine administration. In addition, berberine enhanced autophagy in hypertrophic hearts, which was accompanied by a decrease in heart size, cardiac apoptosis, and the attenuation of cardiac dysfunction. Furthermore, use of autophagy inhibitor 3-methyladenine (3-MA) blocked berberine-induced autophagy level, and abrogated the protection of berberine against heart hypertrophy, cardiac dysfunction, and apoptosis. Berberine ameliorated TAC-induced endoplasmic reticulum stress, which was also abolished by 3-MA. Moreover, berberine significantly inhibited the upstream signaling of autophagy, such as the mammalian target of rapamycin (mTOR), extracellular signal-regulated kinase (ERK1/2), and p38 mitogen-activated protein kinase (MAPK) phosphorylation. We conclude that berberine could attenuate left ventricular remodeling and cardiomyocyte apoptosis through an autophagy-dependent mechanism in a rat model of cardiac hypertrophy, which is, at least in part, associated with enhanced autophagy through inhibition of mTOR, p38 and ERK1/2 MAPK signaling pathways.
European journal of pharmacology.Eur J Pharmacol.2014 Apr 5;728:67-76. doi: 10.1016/j.ejphar.2014.01.061. Epub 2014 Feb 6.
Cardiac hypertrophy is a maladaptive change in response to pressure overload, and is also an important risk for developing heart failure. Berberine is known to have cardioprotective effects in patients with hypertension and in animal models of cardiac hypertrophy. In the current study, we observed t
PMID 24508518

Japanese Journal

子宮内環境のマーカーとしての臍帯動脈血ナトリウム利尿ペプチドホルモンの検討

大坪善数,吉村未央,後田洋子,徳富友紀,合田裕治,角至一郎,上玉利彰,中下誠郎
日本小児科学会雑誌 115(10), 1543-1549, 2011-10-01
NAID 10029836416

Determinants of plasma brain natriuretic peptide levels in untreated hypertensive patients

GODA Akiko,NAKAO Shinji,TSUJINO Takeshi,YUBA Masao,OTSUKA Misato,MATSUMOTO Mika,YOSHIDA Chikako,NAITO Yoshiro,LEE-KAWABATA Masaaki,OHYANAGI Mitsumasa,MASUYAMA Tohru
Journal of echocardiography : official publication of the Japanese Society of Echocardiography 9(3), 103-108, 2011-09-28
NAID 10029728217

Related Pictures

★リンクテーブル★

リンク元	「脳性ナトリウム利尿ペプチド」
関連記事	「natriuretic」「natriuretic peptide」「brain」

「脳性ナトリウム利尿ペプチド」

Natriuretic peptide B
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1YK1, 3N56
Identifiers
Symbols	NPPB; BNP
External IDs	OMIM: 600295 HomoloGene: 81698 GeneCards: NPPB Gene
Gene Ontology
Molecular function	• receptor binding; • hormone activity; • diuretic hormone activity; • peptide hormone receptor binding;
Cellular component	• extracellular region; • extracellular space; • nucleus; • perinuclear region of cytoplasm;
Biological process	• response to hypoxia; • cGMP biosynthetic process; • inflammatory response; • cell surface receptor signaling pathway; • receptor guanylyl cyclase signaling pathway; • heart development; • body fluid secretion; • regulation of blood pressure; • response to organic cyclic compound; • negative regulation of angiogenesis; • negative regulation of cell growth; • positive regulation of urine volume; • positive regulation of renal sodium excretion; • regulation of vasodilation; • response to drug; • regulation of vascular permeability; • response to peptide hormone stimulus; • negative regulation of smooth muscle cell proliferation; • regulation of blood vessel size; • response to calcium ion;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	This box: view; talk; edit;

　　[★]

英: brain natriuretic peptide, BNP
同: 脳ナトリウム利尿ペプチド, B型ナトリウム利尿ペプチド B-type natriuretic peptide

概念

うっ血性心不全のマーカーとして有用
最初、脳で見いだされたが、主に心室から分泌されることが明らかとなった。

基準値

≦20 pg/ml (P+EDTA) (LAB.1797)

分類

性状

ペプチド

産生組織

(主に)心室

標的組織

受容体

ナトリウム利尿ペプチド受容体

作用

ナトリウム利尿作用
血管平滑筋弛緩
交感神経抑制
RAA系抑制

分泌の調整

分子機構

生合成

臨床関連

心機能の評価

心房細動の予後の決定：ANP≧40pg/ml かつ BNP ≦ 200pg/mlであること　→　BNPは左室拡張末期圧と相関。BNPが低値の時は心房の圧負荷が軽度といわれている。

心疾患のマーカー

参考1

	心不全の可能性はきわめて低い	心不全の可能性は低いが、可能ならば経過観察	軽度の心不全の可能性があるので精査、経過観察	治療対象となる心不全の可能性有り精査 or 専門医紹介	治療対象となる心不全の可能性高精査 or 専門医紹介
BNP	0～18.4	18.4～40	40～100	100～200	200～
NT-proBNP	0～125		125～400	400～900	900～

参考

1. 日本心不全学会　ステートメント

http://www.asas.or.jp/jhfs/topics/bnp201300403.html

2. 東京医科大学　救急医学

http://eccm.tokyo-med.ac.jp/report/hachioji/study_6.html

「natriuretic」

　　[★]

ナトリウム利尿の、ナトリウム排泄増加の

関: natriuresis

「natriuretic peptide」

　　[★]

ナトリウム利尿ペプチド

「brain」

　　[★] 脳

[1] Ziskoven D, Forssmann WG, Holthausen U, Menz G, Addicks K, Rippegater G: Calcium Calmodulinantagonists Influences the release of Cardiodilatin/ANP from Atrial Cardiocytes. Handbook Endocrinology of the Heart, edited by Kaufmann W, Wambach G, 01/1989; Springer Verlag Berlin Heidelberg New York; ISBN/EAN 978-3-540-51409-1

[pmid12124404-2] Maisel A, Krishnaswamy P, Nowak R, McCord J, Hollander J, Duc P, Omland T, Storrow A, Abraham W, Wu A, Clopton P, Steg P, Westheim A, Knudsen C, Perez A, Kazanegra R, Herrmann H, McCullough P (2002). "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure". N Engl J Med 347 (3): 161–7. doi:10.1056/NEJMoa020233. PMID 12124404.

[pmid14872150-3] Bhalla V, Willis S, Maisel AS (2004). "B-type natriuretic peptide: the level and the drug--partners in the diagnosis of congestive heart failure". Congest Heart Fail 10 (1 Suppl 1): 3–27. doi:10.1111/j.1527-5299.2004.03310.x. PMID 14872150.

[pmid15389242-4] Atisha D, Bhalla MA, Morrison LK, Felicio L, Clopton P, Gardetto N, Kazanegra R, Chiu A, Maisel AS (September 2004). "A prospective study in search of an optimal B-natriuretic peptide level to screen patients for cardiac dysfunction". Am. Heart J. 148 (3): 518–23. doi:10.1016/j.ahj.2004.03.014. PMID 15389242.

[pmid16431187-5] Strunk A, Bhalla V, Clopton P, Nowak RM, McCord J, Hollander JE, Duc P, Storrow AB, Abraham WT, Wu AH, Steg G, Perez A, Kazanegra R, Herrmann HC, Aumont MC, McCullough PA, Maisel A (January 2006). "Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the Breathing Not Properly Multinational Study". Am. J. Med. 119 (1): 69.e1–11. doi:10.1016/j.amjmed.2005.04.029. PMID 16431187.

[pmid16644322-6] Brenden CK, Hollander JE, Guss D, McCullough PA, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Bhalla V, Clopton P, Jesse R, Maisel AS (May 2006). "Gray zone BNP levels in heart failure patients in the emergency department: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study". Am. Heart J. 151 (5): 1006–11. doi:10.1016/j.ahj.2005.10.017. PMID 16644322.

[pmid15337217-7] Bhalla MA, Chiang A, Epshteyn VA, Kazanegra R, Bhalla V, Clopton P, Krishnaswamy P, Morrison LK, Chiu A, Gardetto N, Mudaliar S, Edelman SV, Henry RR, Maisel AS (September 2004). "Prognostic role of B-type natriuretic peptide levels in patients with type 2 diabetes mellitus". J. Am. Coll. Cardiol. 44 (5): 1047–52. doi:10.1016/j.jacc.2004.05.071. PMID 15337217.

[pmid15145114-8] Hutfless R, Kazanegra R, Madani M, Bhalla MA, Tulua-Tata A, Chen A, Clopton P, James C, Chiu A, Maisel AS (May 2004). "Utility of B-type natriuretic peptide in predicting postoperative complications and outcomes in patients undergoing heart surgery". J. Am. Coll. Cardiol. 43 (10): 1873–9. doi:10.1016/j.jacc.2003.12.048. PMID 15145114.

[pmid15364340-9] Maisel A, Hollander JE, Guss D, McCullough P, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Bhalla V, Clopton P, Jesse R (September 2004). "Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT). A multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath". J. Am. Coll. Cardiol. 44 (6): 1328–33. doi:10.1016/j.jacc.2004.06.015. PMID 15364340.

[pmid15752936-10] Bhalla V, Isakson S, Bhalla MA, Lin JP, Clopton P, Gardetto N, Maisel AS (February 2005). "Diagnostic ability of B-type natriuretic peptide and impedance cardiography: testing to identify left ventricular dysfunction in hypertensive patients". Am. J. Hypertens. 18 (2 Pt 2): 73S–81S. doi:10.1016/j.amjhyper.2004.11.044. PMID 15752936.

[pmid19181293-11] Castellanos LR, Bhalla V, Isakson S, Daniels LB, Bhalla MA, Lin JP, Clopton P, Gardetto N, Hoshino M, Chiu A, Fitzgerald R, Maisel AS (February 2009). "B-type natriuretic peptide and impedance cardiography at the time of routine echocardiography predict subsequent heart failure events". J. Card. Fail. 15 (1): 41–7. doi:10.1016/j.cardfail.2008.09.003. PMID 19181293.

[pmid16098869-12] Resnik JL, Hong C, Resnik R, Kazanegra R, Beede J, Bhalla V, Maisel A (August 2005). "Evaluation of B-type natriuretic peptide (BNP) levels in normal and preeclamptic women". Am. J. Obstet. Gynecol. 193 (2): 450–4. doi:10.1016/j.ajog.2004.12.006. PMID 16098869.

[pmid15286561-13] Bhalla V, Bhalla MA, Maisel AS (August 2004). "Evolution of B-type natriuretic peptide in evaluation of intensive care unit shock". Crit. Care Med. 32 (8): 1787–9. doi:10.1097/01.CCM.0000135748.75590.54. PMID 15286561.

[pmid17239684-14] Sheen V, Bhalla V, Tulua-Tata A, Bhalla MA, Weiss D, Chiu A, Abdeen O, Mullaney S, Maisel A (February 2007). "The use of B-type natriuretic peptide to assess volume status in patients with end-stage renal disease". Am. Heart J. 153 (2): 244.e1–5. doi:10.1016/j.ahj.2006.10.041. PMID 17239684.

[pmid15199359-15] Maisel AS, Clopton P, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, Omland T, Storrow AB, Abraham WT, Wu AH, Steg G, Westheim A, Knudsen CW, Perez A, Kazanegra R, Bhalla V, Herrmann HC, Aumont MC, McCullough PA (June 2004). "Impact of age, race, and sex on the ability of B-type natriuretic peptide to aid in the emergency diagnosis of heart failure: results from the Breathing Not Properly (BNP) multinational study". Am. Heart J. 147 (6): 1078–84. doi:10.1016/j.ahj.2004.01.013. PMID 15199359.

[pmid16679261-16] Daniels LB, Bhalla V, Clopton P, Hollander JE, Guss D, McCullough PA, Nowak R, Green G, Saltzberg M, Ellison SR, Bhalla MA, Jesse R, Maisel A (May 2006). "B-type natriuretic peptide (BNP) levels and ethnic disparities in perceived severity of heart failure: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study of BNP levels and emergency department decision making in patients presenting with shortness of breath". J. Card. Fail. 12 (4): 281–5. doi:10.1016/j.cardfail.2006.01.008. PMID 16679261.

[University_of_Iowa_Department_of_Pathology_Laboratory_Services_Handbook-17] "N-terminal pro-BNP".

[pmid16938661-18] Austin WJ, Bhalla V, Hernandez-Arce I, Isakson SR, Beede J, Clopton P, Maisel AS, Fitzgerald RL (October 2006). "Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease". Am. J. Clin. Pathol. 126 (4): 506–12. doi:10.1309/M7AAXA0J1THMNCDF. PMID 16938661.

[19] Daniels, LB; Clopton, P; Bhalla, V; Krishnaswamy, P; Nowak, RM; McCord, J; Hollander, JE; Duc, P et al. (May 2006). "Results from the Breathing Not Properly Multinational Study". Am. Heart J. 151 (5): 999–1005. doi:10.1016/j.ahj.2005.10.011. PMID 16644321.

[sfhl-20] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p Saint Francis Hospital Laboratory > BNP reference range change Jay Hupp & Dr. Michel S. Medawar. Effective November, 2002

[21] Lam, LL; Cameron, PA; Schneider, HG; Abramson, MJ; Müller, C; Krum, H (2010). "Meta-analysis: effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting". Annals of internal medicine 153 (11): 728–35. doi:10.1059/0003-4819-153-11-201012070-00006. PMID 21135296.

[pmid17213400-22] Bibbins-Domingo K, Gupta R, Na B, Wu AH, Schiller NB, Whooley MA (January 2007). "N-terminal fragment of the prohormone brain-type natriuretic peptide (NT-proBNP), cardiovascular events, and mortality in patients with stable coronary heart disease". JAMA 297 (2): 169–76. doi:10.1001/jama.297.2.169. PMC 2848442. PMID 17213400.

[pmid16169326-23] Fitzgerald RL, Cremo R, Gardetto N, Chiu A, Clopton P, Bhalla V, Maisel AS (September 2005). "Effect of nesiritide in combination with standard therapy on serum concentrations of natriuretic peptides in patients admitted for decompensated congestive heart failure". Am. Heart J. 150 (3): 471–7. doi:10.1016/j.ahj.2004.11.021. PMID 16169326.

[Wang-24] Wang TJ, Larson MG, Levy D, et al. (2004). "Impact of obesity on plasma natriuretic peptide levels". Circulation. 109 (5): 594–600. doi:10.1161/01.CIR.0000112582.16683.EA. PMID 14769680.

[25] Diagnostic Pearls in Cardiorespiratory Disease. CVMA Yosemite Conference 2010. Bruce Keene, DVM, MSc, DACVIM (Cardiology)

[26] O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. The New England journal of medicine 2011;365:32-43.

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brain natriuretic peptide