Natriuretic peptide family consists of several hormones produced by cardiomyocyte, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). They possess similar gene structures and protective effects of cardiovascular physiology, such as anti-hypertrophy, anti-fibrosis, myocardial relaxation and blood pressure regulation. The corresponding natriuretic peptide receptor A, B and C mediate multiple effects of natriuretic peptides to maintain cardiovascular homeostasis. Specially, natriuretic peptide receptor-A preferentially binds ANP and BNP, while natriuretic peptide receptor-B is more selective for C-type natriuretic peptides. Natriuretic peptide recep-tor-C(NPR-C), binding all kinds of natriuretic peptides, clears natriuretic peptides from the circulation through recep-tor-mediated internalization and degradation. BNP levels were reported to be a good predictor of left ventricular dysfunc-tion and decompensated heart failure from a clinical standpoint. BNP infusion is an effective treatment for acute heart fail-ure. Investigations on natriuretic peptides’ single nucleotide polymorphisms and biological function suggested that they could be associated with several cardiovascular diseases, such as atrial fibrillation, cardiomyopathy, heart failure and so on. Transgenic mice with natriuretic peptides and their receptors gene deletion display myocardial hypertrophy and fibrosis, which are associated with the development of hypertension, cardiomyopathy and heart failure. Certain stimuli triggering cardiac hypertrophy and ischemic injuries may be involved in regulating gene expression of natriuretic peptides and their receptors. Therefore, advances in understanding of natriuretic peptide family genes and their regulatory mechanisms will lead to greater insight into the pathogenesis of cardiovascular diseases and blaze a new trail in clinical treatment.
[1] Kapoun AM, Liang FQ, O'Young G, Damm DL, Quon D, White RT, Munson K, Lam A, Schreiner GF, Protter AA. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-β in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation. Circ Res, 2004, 94(4): 453-461.
[2] de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. A rapid and potent natriuretic response to intravenous injec-tion of atrial myocardial extract in rats. Life Sci, 1981, 28(1): 89-94.
[3] Chan JCY, Knudson O, Wu FY, Morser J, Dole WP, Wu QY. Hypertension in mice lacking the proatrial natriuretic peptide convertase corin. Proc Natl Acad Sci USA, 2005, 102(3): 785-790.
[4] Hodgson-Zingman DM, Karst ML, Zingman LV, Heublein DM, Darbar D, Herron KJ, Ballew JD, de Andrade M, Burnett JC Jr, Olson TM. Atrial natriuretic peptide frameshift mutation in familial atrial fibrillation. N Engl J Med, 2008, 359(2): 158-165.
[5] Stambler BS, Guo GB. Atrial natriuretic peptide has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization in anesthetized dogs. J Cardiovasc Electrophysiol, 2005, 16(12): 1341-1347.
[6] Potter LR, Abbey-Hosch S, Dickey DM. Natriuretic peptides, their receptors, and cyclic guanosine monophos-phate-dependent signaling functions. Endocr Rev, 2006, 27(1): 47-72.
[7] Murad F. Shattuck Lecture. Nitric oxide and cyclic GMP in cell signaling and drug development. N Engl J Med, 2006, 355(19): 2003-2011.
[8] Conen D, Glynn RJ, Buring JE, Ridker PM, Zee RYL. Natriuretic peptide precursor a gene polymorphisms and risk of blood pressure progression and incident hypertension. Hypertension, 2007, 50(6): 1114-1119.
[9] Potter LR, Yoder AR, Flora DR, Antos LK, Dickey DM. Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handb Exp Pharmacol, 2009, 191: 341-366.
[10] Schillinger KJ, Tsai SY, Taffet GE, Reddy AK, Marian AJ, Entman ML, Oka K, Chan L, O'Malley BW. Regulatable atrial natriuretic peptide gene therapy for hypertension. Proc Natl Acad Sci USA, 2005, 102(39): 13789-13794.
[11] Felker GM, Petersen JW, Mark DB. Natriuretic peptides in the diagnosis and management of heart failure. Cmaj, 2006, 175(6): 611-617.
[12] See R, de Lemos JA. Current status of risk stratification methods in acute coronary syndromes. Curr Cardiol Rep, 2006, 8(4): 282-288.
[13] Jaffe AS, Babuin L, Apple FS. Biomarkers in acute car-diac disease: the present and the future. J Am Coll Cardiol, 2006, 48(1): 1-11.
[14] Del Greco MF, Pattaro C, Luchner A, Pichler I, Winkler T, Hicks AA, Fuchsberger C, Franke A, Melville SA, Peters A, Wichmann HE, Schreiber S, Heid IM, Krawczak M, Minelli C, Wiedermann CJ, Pramstaller PP. Genome-wide association analysis and fine mapping of NT-proBNP level provide novel insight into the role of the MTHFR-CLCN6-NPPA-NPPB gene cluster. Hum Mol Genet, 2011, 20(8): 1660-1671.
[15] Newton-Cheh C, Larson MG, Vasan RS, Levy D, Bloch KD, Surti A, Guiducci C, Kathiresan S, Benjamin EJ, Struck J, Morgenthaler NG, Bergmann A, Blankenberg S, Kee F, Nilsson P, Yin X, Peltonen L, Vartiainen E, Salo-maa V, Hirschhorn JN, Melander O, Wang TJ. Association of common variants in NPPA and NPPB with circulating natriuretic peptides and blood pressure. Nat Genet, 2009, 41(3): 348-353.
[16] Lajer M, Tarnow L, Jorsal A, Parving HH. Polymorphisms in the B-type natriuretic peptide (BNP) gene are associated with NT-proBNP levels but not with diabetic neph-ropathy or mortality in type 1 diabetic patients. Nephrol Dial Transplant, 2007, 22(11): 3235-3239.
[17] Vassalle C, Andreassi MG, Prontera C, Fontana M, Zyw L, Passino C, Emdin M. Influence of ScaI and natriuretic peptide (NP) clearance receptor polymorphisms o
