Komorski natriuretski peptid

NPPB
Dostupne strukture
PDB	Pretraga ortologa: PDBe RCSB
Spisak PDB ID kodova
	3N56, 1YK1
Identifikatori
Aliasi	NPPB
Vanjski ID-jevi	OMIM: 600295 MGI: 97368 HomoloGene: 81698 GeneCards: NPPB
Lokacija gena (čovjek)
Hrom.	Hromosom 1 (čovjek)
Kraj	11,858,945 bp
Lokacija gena (miš)
Hrom.	Hromosom 4 (miš)
Kraj	148,071,662 bp
Obrazac RNK ekspresije
	Više referentnih podataka o ekspresiji
Ontologija gena
Molekularna funkcija	• GO:0001948, GO:0016582 vezivanje za proteine; • hormone activity; • signaling receptor binding; • diuretic hormone activity; • hormone receptor binding;
Ćelijska komponenta	• extracellular region; • Vanćelijsko; • GO:0009327 makromolekulani kompleks; • jedro; • citoplazma;
Biološki proces	• blood vessel diameter maintenance; • Savijanje proteina; • regulation of signaling receptor activity; • negative regulation of systemic arterial blood pressure; • neuropeptide signaling pathway; • cGMP-mediated signaling; • regulation of blood pressure; • negative regulation of angiogenesis; • cell surface receptor signaling pathway; • regulation of vascular permeability; • receptor guanylyl cyclase signaling pathway; • body fluid secretion; • antimicrobial humoral immune response mediated by antimicrobial peptide; • cGMP biosynthetic process; • negative regulation of cell growth; • positive regulation of urine volume; • positive regulation of renal sodium excretion;
	Izvori:Amigo / QuickGO
Ortolozi
	4879
	18158
	ENSG00000120937
	ENSMUSG00000029019
	P16860
	P40753
	NM_002521
	NM_001287348; NM_008726
	NP_002512; NP_002512
	NP_001274277; NP_032752
	Wikipodaci
Pogledaj/uredi – čovjek	Pogledaj/uredi – miš

Komorski natriuretski peptid ili ventrikulski natriuretski pepid ili moždani natriuretski peptid (BNP) – poznat i kao natriuretski peptid B-tip – je hormon kojeg luče kardiomiociti u srčanoj komori, kao odgovor na istezanje uzrokovano povećanim volumenom komorske krvi. To je 32-aminokiselinski polipeptid BNP, koji se luči se vezan za fragment 76 – aminokiselinskog N-terminal u prohormonu zvanom NT-proBNP (BNPT), koji je biološki neaktivan. Kada je oslobođen, BNP se veže i aktivira pretkomorski receptor natriuretskog faktora NPRA, a u manjoj mjeri NPRB, na način sličan pretkomorskom natriuretskom peptidu (ANP), ali sa 10 puta manjim afinitetom. Međutim, biološko poluvrijeme BNP-a dvostruko je duže od ANP-a, a za NT-proBNP je čak i duže, što za dijagnostiku testiranje krvi, ove peptide čini boljom metom od ANP-a.

Fiziološka dejstva BNP-a slična su djelovanju ANP-a i uključuju smanjenje sistemski vaskularni otpor i centralni venski pritisak, kao i porast natriureze. Neto učinak ovih peptida je smanjenje krvnog pritiska, uslijed smanjenja sistemskog vaskularnog otpora i, prema tome, naknadnog opterećenja. Pored toga, djelovanje BNP-a i ANP-a rezultira smanjenjem minutnog volumena zbog ukupnog smanjenja centralnog venskog pritiska i predopterećenja, kao posljedice smanjenja volumena krvi koji slijedi nakon natriureze i diureze.^[5]

Biosinteza

BNP se sintetizira kao prethormon sa 134 aminokiseline (preproBNP), kodiran ljudskim genom NPPB. Uklanjanjem N-terminalnog signalnog peptida sa 25 ostataka stvara se prohormon, proBNP, koji se skladišti unutarćelijski, kao O-vezani glikoprotein; proBNP se naknadno cijepa između arginina-102 i serina-103, specifičnom konvertazom (vjerovatno furin ili korin) u NT-proBNP i biološki aktivni polipeptid 32-aminokiselinskog BNP-32, koji se luče u krv u ekvimolarnim količinama.^[6] Cepanjem na drugim lokacijama nastaju kraći BNP peptidi, sa nepoznatom biološkom aktivnošću.^[7] Prerada proBNP može se regulirati O-glikozilacijom ostataka u blizini mjesta cijepanja.^[8]

Fiziološki efekti

Budući da se djelovanje BNP-a posreduje putem ANP receptora, fiziološki efekti BNP-a identični su djelovanju ANP-a. Oni će biti ovdje prikazani.

Vezanje na receptor – agonist uzrokuje smanjenje bubrežnu resorpciju natrija, što rezultira smanjenim volumenom krvi. Sekundarni efekti mogu biti poboljšanje srčane frakcije pumpanja i smanjenje sistemskog krvnog pritiska. Također je povećana lipoliza.

Bubrežni

Proširuje aferentnu, a sužava eferentnu glomerulsku arteriolu i opušta mezangijnu ćeliju. Ovo povećava pritisak u glomerulskim kapilarima, povećavajući tako brzinu glomerulske filtracije (GFR), što rezultira većim opterećenjem filtracije natrija i vode.
Povećava protok krvi kroz vasa recta (práve sudove), koji ispraju otopljene materije (NaCl i urea) iz sržnog intersticija.^[9] Niža osmolarnost medulskog (sržnog) intersticija dovodi do manje reapsorpcije tubulske tečnosti i povećanog izlučivanja.
Smanjuje reapsorpciju natrija u distalnom djrlu savijenog tubula (interakcija sa NCC)

^[10] i korin sabirni kanal nefrona, putem gvanozin 3 ', 5'-cikličnog monofosfata (cGMP) zavisna fosforilacija ENaC.

Inhibira lučenje renina, čime inhibira sistem renin-angiotenzin-aldosteron.

Nadbubrežni

Smanjuje lučenje aldosterona u zona glomerulosa kore nadbubrežne žlijezde.

Vaskularni

Opušta glatke mišiće krvnih žila u arteriolama i venama:

Povećava razinu cGMP vaskularnih glatkih mišića posredovanih receptorom;
Inhibira dejstva kateholamina;
Promovira preuređivanje spiralne arterije maternice, što je važno za prevenciju hipertenzije izazvane trudnoćom.^[11]

Srčani

Inhibira neprilagođenu hipertrofiju srca;
Miševi kojima nedostaje srčana NPRA razvijaju povećanu srčanu masu i tešku fibrozu i iznenada uginu;^[12]
Ponovna ekspresija NPRA spašava fenotip.

Masno tkivo

Povećava oslobađanje slobodnih masnih kiselina iz masnog tkiva. Koncentracije glicerola i nesterificiranih masnih kiselina u plazmi povećavaju se intravenskom infuzijom ANP-a na ljudima.
Aktivira adipocitne plazmatske membrane tipa A gvanilil-ciklaznih receptora NPR-A.
Povećava unutarćelijske nivoe cGMP, koji induciraju fosforilaciju na hormon-osetljivu lipazu i perilipin A, aktivacijom cGMP-zavisne protein kinaze - I (cGK-I)
Ne modulira proizvodnju cAMP-a ili aktivnost PKA.

Mjerenje

Za mjerenje BNP i NT-proBNP primjenjuje se imunoesej.^[13]

Tumačenje BNP-a

Glavna klinička korist BNP-a ili NT-proBNP-a je ta što normalan nivo pomaže u isključivanju hroničnog zatajenja srca u hitnim uvjetima. Povišeni BNP ili NT-proBNP nikada se ne smiju koristiti isključivo za "presudu" akutnog ili hroničnog zatajenja srca u hitnim uvjetima, zbog nedostka specifičnosti.^[14]
BNP ili NT-proBNP takođe se mogu koristiti za skrining i prognozu zatajenja srca.^[15]
BNP i NT-proBNP također su uobičajeno povećani kod pacijenata s disfunkcijom lijeve komore, sa ili bez simptoma (BNP tačno odražava aktuelni status srčane komore, budući da mu je poluživot 20 minuta, za razliku od 1-2 sata za NT-proBNP).^[16]

Preoperativni BNP može predvidjeti rizik od akutnih srčanih događaja tokom vaskularne hirurgije. Granična vrednost od 100 pg / ml ima osetljivost od približno 100%, negativnu prediktivnu vrijednost od približno 100%, a specifičnost od 90% i pozitivnu prediktivnu vrijrdnost od 78%, prema podacima iz Ujedinjenog Kraljevstva.^[17]

BNP se uklanja vezanjem za natriuretske peptidne receptore (NPR) i neutralnu endopeptidazu (NEP). Manje od 5% BNP-a uklanja se bubrežno. NT-proBNP je neaktivna molekula koja nastaje cijepanjem prohormona Pro-BNP i za izlučivanje se oslanja isključivo na bubreg. Ahilova peta, odnosno slaba tačka molekule NT-proBNP preklapa se u bolesti bubrega u populaciji pacijenata sa srčanom insuficijencijomBNP is cleared by binding to natriuretic peptide receptors (NPRs) and neutral endopeptidase (NEP).^[18]^[19]

Utvrđeno je da je, kod muškaraca, nizak BNP dobar prediktor za preživljavanje do 90 godina.^[20]

Neke laboratorije izvještavaju u jedinicama ng po litru (ng/L), što je ekvivalentno pg/ml.

Postoji dijagnostička „siva zona“, koja se često definira kao raspon između 100 i 500 pg/ml, za koju se test smatra neuvjerljivim, ali, općenito, razine iznad 500 pg/ml smatraju se pokazateljem zatajenja srca. Ova takozvana siva zona obrađivana je u nekoliko studija, a u postavljanju dijagnoze može pomoći upotreba kliničke historije ili drugih dostupnih jednostavnih alata.^[21]^[22]

BNP može biti pouzdan prediktor kardiovaskularne smrtnosti kod dijabetičara.^[23]

Utvrđeno je da BNP ima važnu ulogu u prognoziranju pacijenata kojima je neophodna srčana hirurgija^[24] i služba hitne pomoći.^[25] Bhalla et al. pokazali su da kombiniranje BNP-a s drugim alatima poput ICG-a može poboljšati ranu dijagnozu zatajenja srca i unaprijediti strategije prevencije.^[26]^[27] Korisnost BNP-a također je istražena u raznim postavkama poput preeklampsije, ICU-a, šoka i ESRD-a.^[28]^[29]^[30]

Opsežno su proučavani veze „rasno“-populacijske i spolne pripadnosti na vrijednost BNP-a i njegove korisnosti u tom kontekstu.^[31]^[32]

Razune NT-proBNP (u pg/mL) po klasama funkcije NYHA ^[33]
	NYHA I	NYHA II	NYHA III	NYHA IV
Vjerovatnoćs 5%	33	103	126	148
Prosjek	1015	1666	3029	3465
Vjerovatnoća 95%	3410	6567	10,449	12,188

BNP-test koristi se kao pomoć u dijagnozi i procjeni ozbiljnosti srčanog zatajenja. Nedavna metaanaliza u vezi s učincima BNP testiranja na kliničke ishode pacijenata koji se javljaju na odjel hitne pomoći s akutnom dispnejom, otkrila je da je BNP testiranje dovelo do smanjenja stopa prijema i smanjenja srednje dužine boravka, iako nijedno nije bilo statistički značajno. Efekti na smrtnost iz svih razloga u bolnici nisu bili konačni.^[34] BNP test se također koristi za raslojavanje rizika pacijenata sa akutnim koronarnim sindromima.^[35]^[36]

Pri tumačenju povišenog nivoa BNP, korisno je znati da vrijednosti mogu biti povišene zbog faktora koji nisu srčana insuficijencija. Niži nivo se često primećuje kod gojaznih pacijenata.^[37] Higher levels are seen in those with renal disease, in the absence of heart failure.

Terapijska primjena

Rekombinantni BNP, nesiritid, predložen je kao tretman za dekompenzirano zatajenje srca. Međutim, kliničko ispitivanje^[38] nije pokazao korist nesiritida kod pacijenata sa akutnim dekompenziranim zatajenjem srca. Blokada neprilisinske proteaze za koju je poznato da razgrađuje članove porodice natriuretičkih peptida, takođe je predložena kao mogući način liječenja zatajenja srca. Pokazalo se da je dvostruka primjena inhibitora neprilisina i blokatora angiotenzinskih receptora korisna za ACE inhibitor, trenutnu terapiju prve linije, u više postavki.^[39]^[40]

Također pogledajte

Reference

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^ Fitzgerald RL, Cremo R, Gardetto N, Chiu A, Clopton P, Bhalla V, Maisel AS (septembar 2005). "Effect of nesiritide in combination with standard therapy on serum concentrations of natriuretic peptides in patients admitted for decompensated congestive heart failure". American Heart Journal. 150 (3): 471–7. doi:10.1016/j.ahj.2004.11.021. PMID 16169326.
^ Wang TJ, Larson MG, Levy D, Benjamin EJ, Leip EP, Wilson PW, Vasan RS (februar 2004). "Impact of obesity on plasma natriuretic peptide levels". Circulation. 109 (5): 594–600. doi:10.1161/01.CIR.0000112582.16683.EA. PMID 14769680.
^ O'Connor CM, Starling RC, Hernandez AF, Armstrong PW, Dickstein K, Hasselblad V, et al. (juli 2011). "Effect of nesiritide in patients with acute decompensated heart failure" (PDF). The New England Journal of Medicine. 365 (1): 32–43. doi:10.1056/NEJMoa1100171. hdl:11379/60663. PMID 21732835.
^ McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, Rouleau JL, Shi VC, Solomon SD, Swedberg K, Zile MR (septembar 2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". The New England Journal of Medicine. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. hdl:10993/27659. PMID 25176015.
^ Velazquez EJ, Morrow DA, DeVore AD, Duffy CI, Ambrosy AP, McCague K, Rocha R, Braunwald E (februar 2019). "Angiotensin-Neprilysin Inhibition in Acute Decompensated Heart Failure". The New England Journal of Medicine. 380 (6): 539–548. doi:10.1056/NEJMoa1812851. PMID 30415601.

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Vanjski linkovi

Brain Natriuretic Peptide na US National Library of Medicine Medical Subject Headings (MeSH)
BNP and NT-proBNP at Lab Tests Online Arhivirano 28. 7. 2017. na Wayback Machine

Commons logo

Commons ima datoteke na temu: Komorski natriuretski peptid

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000120937 - Ensembl, maj 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000029019 - Ensembl, maj 2017

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[Wang-37] Wang TJ, Larson MG, Levy D, Benjamin EJ, Leip EP, Wilson PW, Vasan RS (februar 2004). "Impact of obesity on plasma natriuretic peptide levels". Circulation. 109 (5): 594–600. doi:10.1161/01.CIR.0000112582.16683.EA. PMID 14769680.

[pmid21732835-38] O'Connor CM, Starling RC, Hernandez AF, Armstrong PW, Dickstein K, Hasselblad V, et al. (juli 2011). "Effect of nesiritide in patients with acute decompensated heart failure" (PDF). The New England Journal of Medicine. 365 (1): 32–43. doi:10.1056/NEJMoa1100171. hdl:11379/60663. PMID 21732835.

[39] McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, Rouleau JL, Shi VC, Solomon SD, Swedberg K, Zile MR (septembar 2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". The New England Journal of Medicine. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. hdl:10993/27659. PMID 25176015.

[40] Velazquez EJ, Morrow DA, DeVore AD, Duffy CI, Ambrosy AP, McCague K, Rocha R, Braunwald E (februar 2019). "Angiotensin-Neprilysin Inhibition in Acute Decompensated Heart Failure". The New England Journal of Medicine. 380 (6): 539–548. doi:10.1056/NEJMoa1812851. PMID 30415601.

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