Pretkomorski natriuretski peptid

Pretkomorski natriuretski peptid
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Pogledaj/uredi – čovjek

Komorski natriuretski peptid ili moždani natriuretski peptid (BNP) – poznat i kao B-tip natriuretskog peptida – je hormon kojeg luče s kardiomiociti u srčanoj komori, kao odgovor na istezanje uzrokovano povećanim volumenom komorske krvi.

Lučenje 32-aminokiselinskog polipeptid BNP vezano je za fragment od 76-aminokiselinskog N-terminala u prohormonu zvanom NT-proBNP (BNPT), koji je biološki neaktivan. Oslobođeni BNP veže i aktivira atrijski receptor natriuretskog faktora NPRA, a u manjoj mjeri i NPRB, slično atrijskom natriuretskom peptidu (ANP), ali sa 10 puta manjim afinitetom. Međutim, biološki poluvrijeme BNP-a dvostruko je duže od ANP-a, a za NT-proBNP je čak i duže, čineći ove peptide boljom metom od ANP-a za dijagnostiku testiranja krvi.

Fiziološko djelovanje BNP-a slično je djelovanju ANP-a i uključuje smanjenje sistemskog vaskularnog otpora i centralnog venskog pritiska, 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 i BNP i ANP rezultira smanjenjem minutnog volumena zbog ukupnog smanjenja centralnog venskog pritiska i predopterećenja, kao rezultat smanjenja volumena krvi koji slijedi nakon natriureze i diureze.^[1]

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 luči u krv u ekvimolarnim količinama.^[2] Cleavage at other sites produces shorter BNP peptides with unknown biological activity.^[3] Prerada proBNP može se regulirati O-glikozilacijom ostataka u blizini mjesta cijepanja.^[4]

Fiziološki efekti

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

Veznje na receptor – agonist uzrokuje smanjenje resorpciju bubrežnog natrija, što rezultira smanjenje volumena krvi. Sekundarni efekti mogu biti poboljšanje srčane frakcije ispumpavanja i smanjenje sistemskog krvnog pritiska. Također je povećana i lipoliza.

Bubrežni

Proširuje aferentnu glomerulsku arteriolu, sužava eferentnu glomerularnu arteriolu i opušta mezangijne ćelije. Ovo povećava pritisak u glomerulskih kapilara, povećavajući tako brzinu glomerulne filtracije (GFR), što rezultira većim opterećenjem natrija i vode u filtratu.
Povećava protok krvi kroz vasa recta (uspravne sudove), koji će isprati otopljene materije (NaCl i urea) iz sržnog intersticija.^[5] Niža osmolarnost sržnog bubrežnog intersticija dovodi do manje reapsorpcije tubulske tečnosti i povećanog izlučivanja.
Smanjuje reapsorpciju natrija u distalnom dijelu savijenog tubula (interakcija sa NCC)^[6] i sabirnih kanala nefrona, putem gvanozin 3', 5'-cikličnog monofosfata (cGMP), zavisna fosforilacija ENaC.
Inhibira lučenje renina, čime koči sistem renin – angiotenzin – aldosteron.

Nadbubrežni

Smanjuje lučenje aldosterona iz zona glomeruloza kore nadbubrežne žlijezde.

Vaskularni

Opušta glatke mišiće krvnih žila u arteriolama i venama:

Povećava cGMP vaskularnih glatkih mišića posredovanih receptorom;
Inhibicira dejstva kateholaminaanda sabirnog kanala bubrežne kore.
Promovira preuređivanje spiralne arterije maternice, što je važno za prevenciju hipertenzije izazvane trudnoćom.^[7]

Srčani

Inhibira neprilagođenu hipertrofiju srca;
Miševi kojima nedostaje srčana NPRA razvijaju povećanu srčanu masu i tešku fibrozu i iznenada uginu;^[8]
Ponovna ekspresija NPRA spašava fenotip.

Adipozni

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 plazamatske membrane, tip A receptora gvanilil ciklaze NPR-A
Povećava unutarćelijske nivoe cGMP koji indukuju fosforilaciju na hormon osetljivu lipazu i perilipin A aktivacijom cGMP-zavisne protein-kinaze – I (cGK-I)
Ne modulira proizvodnju cAMP-a ili aktivnost PKA aktivnost

Mjerenje

BNP i NT-proBNP mjere se imunskim testovima.^[9]

Tumačenje BNP-a

Glavna klinička korisnost BNP-a ili NT-proBNP-a je ta što, u hitnim uvjetima, normalni nivo pomaže u isključivanju hroničnog zatajenja srca. Povišeni BNP ili NT-proBNP nikada se ne bi trebali koristiti isključivo za "presudu" akutnog ili hroničnog zatajenja srca u hitnim uvjetima zbog nedostatka specifičnosti.^[10]
BNP ili NT-proBNP se također mogu koristiti za skrining i prognozu srčanog zatajenja.^[11]
BNP i NT-proBNP također su obično povećani kod pacijenata s disfunkcijom lijeve komore, sa ili bez simptoma (BNP tačno odražava dati status komore, budući da mu je poluživot 20 minuta, za razliku od 1-2 sata kod NT-proBNP).^[12]

Preoperativni BNP može predvidjeti rizik od akutnih srčanih događaja tokom vaskularne hirurgije. Granična vrednost od 100 pg/ml ima osetljivost od približno 100%, negativna prediktivna vrijednost od približno 100%, a specifičnost od 90% i pozitivna prediktivna vrijednost od 78% prema podacima iz Ujedinjenog Kraljevstva.^[13]

Razine NT-proBNP (u pg/mL) prema klasama funkcije NYHA^[14]
	NYHA I	NYHA II	NYHA III	NYHA IV
Vjerovatnoća 5 %	33	103	126	148
Prosjek	1.015	1.666	3.029	3.465
Vjerovatnoča 95 %	3.410	6.567	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 su se pojavili na hitnom odjelu s akutnom dispnejom, otkrila je da je BNP testiranje dovelo do smanjenja stopa prijema i smanjenja srednje dužine boravka, iako nije bilo statistički značajno. Efekti na smrtnost iz svih razloga u bolnici nisu bili konačni.^[15] BNP test se takođe koristi za raslojavanje rizika pacijenata sa akutnim koronarnim sindromima.^[16]^[17]

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.^[18] Viši nivo se opaža kod onih sa bubrežnom bolešću, u odsustvu srčanog zatajenja.

Terapijska primjena

Rekombinantni BNP, nesiritid, predložen je kao tretman za dekompenzirano zatajenje srca. Međutim, kliničko ispitivanje^[19] nije pokazao korist nesiritida kod pacijenata sa akutnim dekompenziranim zatajenjem srca. Blokada neprilizina, proteaze za koju je poznato da razgrađuje članove porodice natriuretskih peptida, također je predložena kao mogući način liječenja zatajenja srca. Pokazalo se da je dvostruka primjena inhibitora neprilisina i blokatora angiotenzinskih receptora korisna za ACE inhibitor, sadašnju terapiju prve linije, u više postavki .^[20]^[21]

Također pogledajte

Bubreg

Reference

^ "CV Pharmacology - Natriuretic Peptides". cvpharmacology.com. Arhivirano s originala, 21. 10. 2017. Pristupljeno 29. 4. 2018.
^ Schellenberger U, O'Rear J, Guzzetta A, Jue RA, Protter AA, Pollitt NS (juli 2006). "The precursor to B-type natriuretic peptide is an O-linked glycoprotein". Archives of Biochemistry and Biophysics. 451 (2): 160–6. doi:10.1016/j.abb.2006.03.028. PMID 16750161.
^ Niederkofler EE, Kiernan UA, O'Rear J, Menon S, Saghir S, Protter AA, Nelson RW, Schellenberger U (novembar 2008). "Detection of endogenous B-type natriuretic peptide at very low concentrations in patients with heart failure". Circulation: Heart Failure. 1 (4): 258–64. doi:10.1161/CIRCHEARTFAILURE.108.790774. PMID 19808300.
^ Semenov AG, Postnikov AB, Tamm NN, Seferian KR, Karpova NS, Bloshchitsyna MN, Koshkina EV, Krasnoselsky MI, Serebryanaya DV, Katrukha AG (mart 2009). "Processing of pro-brain natriuretic peptide is suppressed by O-glycosylation in the region close to the cleavage site". Clinical Chemistry. 55 (3): 489–98. doi:10.1373/clinchem.2008.113373. PMID 19168558.
^ Kiberd BA, Larson TS, Robertson CR, Jamison RL (juni 1987). "Effect of atrial natriuretic peptide on vasa recta blood flow in the rat". The American Journal of Physiology. 252 (6 Pt 2): F1112-7. doi:10.1152/ajprenal.1987.252.6.F1112. PMID 2954471.
^ Reeves WB, Andreoli TE (2008). "Chapter 31 – Sodium Chloride Transport in the Loop of Henle, Distal Convoluted Tubule, and Collecting Duct". u Giebisch GH, Alpern RA, Herbert SC, Seldin DW (ured.). Seldin and Giebisch's the kidney: physiology and pathophysiology. Amsterdam: Elsevier/Academic Press. str. 849–887. doi:10.1016/B978-012088488-9.50034-6. ISBN 978-0-12-088488-9.
^ Cui Y, Wang W, Dong N, Lou J, Srinivasan DK, Cheng W, Huang X, Liu M, Fang C, Peng J, Chen S, Wu S, Liu Z, Dong L, Zhou Y, Wu Q (mart 2012). "Role of corin in trophoblast invasion and uterine spiral artery remodelling in pregnancy". Nature. 484 (7393): 246–50. Bibcode:2012Natur.484..246C. doi:10.1038/nature10897. PMC 3578422. PMID 22437503.
^ Tamura N, Ogawa Y, Chusho H, Nakamura K, Nakao K, Suda M, Kasahara M, Hashimoto R, Katsuura G, Mukoyama M, Itoh H, Saito Y, Tanaka I, Otani H, Katsuki M (april 2000). "Cardiac fibrosis in mice lacking brain natriuretic peptide". Proceedings of the National Academy of Sciences of the United States of America. 97 (8): 4239–44. doi:10.1073/pnas.070371497. PMC 18212. PMID 10737768.
^ Clerico A, Zaninotto M, Prontera C, Giovannini S, Ndreu R, Franzini M, Zucchelli GC, Plebani M (decembar 2012). "State of the art of BNP and NT-proBNP immunoassays: the CardioOrmoCheck study". Clinica Chimica Acta; International Journal of Clinical Chemistry. 414: 112–9. doi:10.1016/j.cca.2012.07.017. PMID 22910582.
^ Maisel AS, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, Omland T, Storrow AB, Abraham WT, Wu AH, Clopton P, Steg PG, Westheim A, Knudsen CW, Perez A, Kazanegra R, Herrmann HC, McCullough PA (juli 2002). "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure". The New England Journal of Medicine. 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". Congestive Heart Failure. 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 (septembar 2004). "A prospective study in search of an optimal B-natriuretic peptide level to screen patients for cardiac dysfunction". American Heart Journal. 148 (3): 518–23. doi:10.1016/j.ahj.2004.03.014. PMID 15389242.
^ Berry C, Kingsmore D, Gibson S, Hole D, Morton JJ, Byrne D, Dargie HJ (mart 2006). "Predictive value of plasma brain natriuretic peptide for cardiac outcome after vascular surgery". Heart. 92 (3): 401–2. doi:10.1136/hrt.2005.060988. PMC 1860808. PMID 16501204.
^ "N-terminal pro-BNP". Arhivirano s originala, 11. 10. 2008.
^ Lam LL, Cameron PA, Schneider HG, Abramson MJ, Müller C, Krum H (decembar 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:10.7326/0003-4819-153-11-201012070-00006. PMID 21135296.
^ Bibbins-Domingo K, Gupta R, Na B, Wu AH, Schiller NB, Whooley MA (januar 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 (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.

Dopunska literatura

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Buchner S, Riegger G, Luchner A (2005). "[Clinical utility of the cardiac markers BNP and NT-proBNP]". Acta Medica Austriaca. 31 (4): 144–51. PMID 15732251.
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Vanjski linkovi

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

Commons logo

Commons ima datoteke na temu: Pretkomorski natriuretski peptid

BNP and NT-proBNP at Lab Tests Online Arhivirano 28. 7. 2017. na Wayback Machine

[1] "CV Pharmacology - Natriuretic Peptides". cvpharmacology.com. Arhivirano s originala, 21. 10. 2017. Pristupljeno 29. 4. 2018.

[pmid16750161-2] Schellenberger U, O'Rear J, Guzzetta A, Jue RA, Protter AA, Pollitt NS (juli 2006). "The precursor to B-type natriuretic peptide is an O-linked glycoprotein". Archives of Biochemistry and Biophysics. 451 (2): 160–6. doi:10.1016/j.abb.2006.03.028. PMID 16750161.

[pmid19808300-3] Niederkofler EE, Kiernan UA, O'Rear J, Menon S, Saghir S, Protter AA, Nelson RW, Schellenberger U (novembar 2008). "Detection of endogenous B-type natriuretic peptide at very low concentrations in patients with heart failure". Circulation: Heart Failure. 1 (4): 258–64. doi:10.1161/CIRCHEARTFAILURE.108.790774. PMID 19808300.

[pmid19168558-4] Semenov AG, Postnikov AB, Tamm NN, Seferian KR, Karpova NS, Bloshchitsyna MN, Koshkina EV, Krasnoselsky MI, Serebryanaya DV, Katrukha AG (mart 2009). "Processing of pro-brain natriuretic peptide is suppressed by O-glycosylation in the region close to the cleavage site". Clinical Chemistry. 55 (3): 489–98. doi:10.1373/clinchem.2008.113373. PMID 19168558.

[pmid2954471-5] Kiberd BA, Larson TS, Robertson CR, Jamison RL (juni 1987). "Effect of atrial natriuretic peptide on vasa recta blood flow in the rat". The American Journal of Physiology. 252 (6 Pt 2): F1112-7. doi:10.1152/ajprenal.1987.252.6.F1112. PMID 2954471.

[isbn0-12-088488-7-6] Reeves WB, Andreoli TE (2008). "Chapter 31 – Sodium Chloride Transport in the Loop of Henle, Distal Convoluted Tubule, and Collecting Duct". u Giebisch GH, Alpern RA, Herbert SC, Seldin DW (ured.). Seldin and Giebisch's the kidney: physiology and pathophysiology. Amsterdam: Elsevier/Academic Press. str. 849–887. doi:10.1016/B978-012088488-9.50034-6. ISBN 978-0-12-088488-9.

[7] Cui Y, Wang W, Dong N, Lou J, Srinivasan DK, Cheng W, Huang X, Liu M, Fang C, Peng J, Chen S, Wu S, Liu Z, Dong L, Zhou Y, Wu Q (mart 2012). "Role of corin in trophoblast invasion and uterine spiral artery remodelling in pregnancy". Nature. 484 (7393): 246–50. Bibcode:2012Natur.484..246C. doi:10.1038/nature10897. PMC 3578422. PMID 22437503.

[8] Tamura N, Ogawa Y, Chusho H, Nakamura K, Nakao K, Suda M, Kasahara M, Hashimoto R, Katsuura G, Mukoyama M, Itoh H, Saito Y, Tanaka I, Otani H, Katsuki M (april 2000). "Cardiac fibrosis in mice lacking brain natriuretic peptide". Proceedings of the National Academy of Sciences of the United States of America. 97 (8): 4239–44. doi:10.1073/pnas.070371497. PMC 18212. PMID 10737768.

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