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Vol 15, No 2 (2020)
Review Papers
Published online: 2020-08-31
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Progress in study on natriuretic peptides

Stanisław Surma, Edward Bańkowski
DOI: 10.5603/FC.2020.0027
·
Folia Cardiologica 2020;15(2):137-148.

open access

Vol 15, No 2 (2020)
Review Papers
Published online: 2020-08-31

Abstract

Natriuretic peptides are hormones mainly involved in the regulation of water and electrolyte balance and the regulation of cardiovascular function. So far, six classic natiruretic peptides have been described: type A natriuretic peptide, type B natriuretic peptide, type C natriuretic peptide, type D natriuretic peptide and uroguanylin. The family of natiruretic peptides also includes osteocrine and musculin, which have different metabolic activities. Natiruretic peptides carry out their biological activities by interacting with three membrane receptors. The bioavailability of these compounds is regulated, among others, by neprilisin. Plasma nartiuretic peptide concentrations change during many diseases. The most important of these include heart failure. The guidelines of the European Society of Cardiology indicate that the determination of plasma natriuretic peptide levels is helpful in the diagnosis of heart failure. Understanding the physiology of natiruretic peptides has led to the search for new drugs that would mimic their beneficial effects. In addition to the beneficial effects of natriuretic peptides on the cardiovascular system, it has been shown that these compounds are involved in the regulation of many other metabolic processes - among others in the regulation of the center of hunger and satiety in the hypothalamus. The purpose of this work is to present the definitions, history, mechanisms of natiruretic peptides, as well as their role in human physiology and pathology and to present clinical issues related to these hormones.

Abstract

Natriuretic peptides are hormones mainly involved in the regulation of water and electrolyte balance and the regulation of cardiovascular function. So far, six classic natiruretic peptides have been described: type A natriuretic peptide, type B natriuretic peptide, type C natriuretic peptide, type D natriuretic peptide and uroguanylin. The family of natiruretic peptides also includes osteocrine and musculin, which have different metabolic activities. Natiruretic peptides carry out their biological activities by interacting with three membrane receptors. The bioavailability of these compounds is regulated, among others, by neprilisin. Plasma nartiuretic peptide concentrations change during many diseases. The most important of these include heart failure. The guidelines of the European Society of Cardiology indicate that the determination of plasma natriuretic peptide levels is helpful in the diagnosis of heart failure. Understanding the physiology of natiruretic peptides has led to the search for new drugs that would mimic their beneficial effects. In addition to the beneficial effects of natriuretic peptides on the cardiovascular system, it has been shown that these compounds are involved in the regulation of many other metabolic processes - among others in the regulation of the center of hunger and satiety in the hypothalamus. The purpose of this work is to present the definitions, history, mechanisms of natiruretic peptides, as well as their role in human physiology and pathology and to present clinical issues related to these hormones.

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Keywords

natriuretic peptides; cardiovascular system; heart failure; cardiovascular diseases

About this article
Title

Progress in study on natriuretic peptides

Journal

Folia Cardiologica

Issue

Vol 15, No 2 (2020)

Pages

137-148

Published online

2020-08-31

DOI

10.5603/FC.2020.0027

Bibliographic record

Folia Cardiologica 2020;15(2):137-148.

Keywords

natriuretic peptides
cardiovascular system
heart failure
cardiovascular diseases

Authors

Stanisław Surma
Edward Bańkowski

References (68)
  1. Rubattu S, Volpe M. Natriuretic peptides in the cardiovascular system: multifaceted roles in physiology, pathology and therapeutics. Int J Mol Sci. 2019; 20(16).
  2. Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl J Med. 1998; 339(5): 321–328.
  3. Thomas G, Moffatt P, Salois P, et al. Osteocrin, a novel bone-specific secreted protein that modulates the osteoblast phenotype. J Biol Chem. 2003; 278(50): 50563–50571.
  4. Nishizawa H, Matsuda M, Yamada Y, et al. Musclin, a novel skeletal muscle-derived secretory factor. J Biol Chem. 2004; 279(19): 19391–19395.
  5. Potter LR, Abbey-Hosch S, Dickey DM. Natriuretic peptides, their receptors, and cyclic guanosine monophosphate-dependent signaling functions. Endocr Rev. 2006; 27(1): 47–72.
  6. Kish B. Electron microscopy af the atrium of the heart. Exp Med Surg. 1956; 14: 99.
  7. Jamieson JD, Palade GE. Specific granules in atrial muscle cels. J Cell Biol. 1964; 23: 151–172.
  8. Genest J, de Bold AJ, Borenstein HB, et al. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats. Life Sci. 1981; 28(1): 89–94.
  9. Lumsden NG, Khambata RS, Hobbs AJ. C-type natriuretic peptide (CNP): cardiovascular roles and potential as a therapeutic target. Curr Pharm Des. 2010; 16(37): 4080–4088.
  10. Schulz-Knappe P, Forssmann K, Herbst F, et al. Isolation and structural analysis of. Klin Wochenschr. 1988; 66(17): 752–759.
  11. Schweitz H, Vigne P, Moinier D, et al. A new member of the natriuretic peptide family is present in the venom of the green mamba (Dendroaspis angusticeps). J Biol Chem. 1992; 267(20): 13928–13932.
  12. Yuge S. Chapter 23 – Guanylin family. In: Takei Y, Ando H, Tsutsui K, Hikaku N, Gakkai N. ed. Handbook of hormones: comparative endocrinology for basic and clinical research. Academic Press, Oxford 2016: 195–196.
  13. Nichols M, Townsend N, Scarborough P, et al. Cardiovascular disease in Europe: epidemiological update. Eur Heart J. 2013; 34(39): 3028–3034.
  14. Zdrojewski T, Solnica B, Cybulska B, et al. Prevalence of lipid abnormalities in Poland. The NATPOL 2011 survey. Kardiol Pol. 2016; 74(3): 213–223.
  15. Surma S, Szyndler A, Narkiewicz K. [Awareness of selected risk factors for cardiovascular disease in the young population] [Article in Polish]. Choroby Serca i Naczyń. 2017; 14(4): 186.
  16. Surma St, Szyndler A, Narkiewicz K. [Awareness of hypertension and other risk factors for cardiovascular disease in the adult population] [Article in Polish]. Choroby Serca i Naczyń. 2018; 15(1): 14–22.
  17. Ponikowski P, Voors A, Anker S, et al. [2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure] [Article in Polish]. Kardiol Pol. 2016; 74(10): 1037–1147.
  18. Nishikimi T, Kuwahara K, Nakao K. Current biochemistry, molecular biology, and clinical relevance of natriuretic peptides. J Cardiol. 2011; 57(2): 131–140.
  19. Jerczyńska H, Pawłowska Z. Peptydy natriuretyczne — ich receptory i rola w układzie krążenia. Post Bioch. 2007; 54: 35–42.
  20. Kerkelä R, Ulvila J, Magga J. Natriuretic peptides in the regulation of cardiovascular physiology and metabolic events. J Am Heart Assoc. 2015; 4(10): e002423.
  21. Vesely DL, Perez-Lamboy GI, Schocken DD. Long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide enhance the urinary excretion rate of beta2-microglobulin. Metabolism. 2000; 49(12): 1592–1597.
  22. Chen HH, Burnett JC. Natriuretic peptides in the pathophysiology of congestive heart failure. Curr Cardiol Rep. 2000; 2(3): 198–205.
  23. Volpe M, Tocci G, Battistoni A, et al. Angiotensin II receptor blocker neprilysin inhibitor (ARNI): new avenues in cardiovascular therapy. High Blood Press Cardiovasc Prev. 2015; 22(3): 241–246.
  24. Stryjewski P, Nessler B, Cubera K, et al. Peptydy natriuretyczne. Historia odkrycia, budowa chemiczna, mechanizmdziałania oraz metabolizm. Podstawy zastosowania diagnostycznego i leczniczego. Przegl Lek. 2013; 70: 463–467.
  25. Szabó G. Biology of the B-type natriuretic peptide: structure, synthesis and processing. Biochem Anal Biochem. 2012; 1(8): 1000e129.
  26. Favresse J, Gruson D. Natriuretic peptides: degradation, circulating forms, dosages and new therapeutic approaches. Ann Biol Clin (Paris). 2017; 75(3): 259–267.
  27. Potter LR, Yoder AR, Flora DR, et al. Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handb Exp Pharmacol. 2009(191): 341–366.
  28. Pandit K, Mukhopadhyay P, Ghosh S, et al. Natriuretic peptides: diagnostic and therapeutic use. Indian J Endocrinol Metab. 2011; 15(Suppl 4): S345–S353.
  29. Rahbi H, Narayan H, Jones DJL, et al. The uroguanylin system and human disease. Clin Sci (Lond). 2012; 123(12): 659–668.
  30. Mannu G, Bhalerao A. Advances in the mechanism of action of natriuretic peptides at a cellular level. BJMMR. 2015; 9(11): 1–15.
  31. Rubattu S, Sciarretta S, Valenti V, et al. Natriuretic peptides: an update on bioactivity, potential therapeutic use, and implication in cardiovascular diseases. Am J Hypertens. 2008; 21(7): 733–741.
  32. Volpe M, Rubattu S, Burnett J. Natriuretic peptides in cardiovascular diseases: current use and perspectives. Eur Heart J. 2014; 35(7): 419–425.
  33. Das BB, Solinger R. Role of natriuretic peptide family in cardiovascular medicine. Cardiovasc Hematol Agents Med Chem. 2009; 7(1): 29–42.
  34. Kario K. The sacubitril/valsartan, a first-in-class, angiotensin receptor neprilysin inhibitor (ARNI): potential uses in hypertension, heart failure, and beyond. Curr Cardiol Rep. 2018; 20(1): 5.
  35. Surma S, Adamczak M, Więcek A. Hiponatremia spowodowana tiazydowymi i tiazydopodobnymi lekami moczopędnymi. Terapia. 2019; 10(381): 4–10.
  36. Demiralay C, Wiedermann K. Influence of exogenous atrial natriuretic peptide on the noctural hypothalamic-pituary-adrenal axis and sleep i healthy men. Psych Neur Endo. 2010; 10: 1438–1445.
  37. Więcek A, Januszewicz A, Szczepańska-Sadowska E. ed. Nadciśnienie tętnicze. Medycyna Praktyczna, Kraków 2018.
  38. Forte M, Madonna M, Schiavon S, et al. Cardiovascular pleiotropic effects of natriuretic peptides. Int J Mol Sci. 2019; 20(16).
  39. Gojowy D, Więcek A. Co nowego w patogenezie nadciśnienia sodozależnego? In: Więcek A. ed. Postępy w nefrologii i nadciśnieniu tętniczym. Medycyna Praktyczna, Kraków 2019: 15–21.
  40. Pandey KN. Genetic ablation and guanylyl cyclase/natriuretic peptide receptor-A: impact on the pathophysiology of cardiovascular dysfunction. Int J Mol Sci. 2019; 20(16).
  41. Bordicchia M, Liu D, Amri EZ, et al. Cardiac natriuretic peptides act via p38 MAPK to induce the brown fat thermogenic program in mouse and human adipocytes. J Clin Invest. 2012; 122(3): 1022–1036.
  42. Bordicchia M, Spannella F, Ferretti G, et al. PCSK9 is expressed in human visceral adipose tissue and regulated by insulin and cardiac natriuretic peptides. Int J Mol Sci. 2019; 20(2).
  43. Lagace TA. PCSK9 and LDLR degradation: regulatory mechanisms in circulation and in cells. Curr Opin Lipidol. 2014; 25(5): 387–393.
  44. Urban D, Pöss J, Böhm M, et al. Targeting the proprotein convertase subtilisin/kexin type 9 for the treatment of dyslipidemia and atherosclerosis. J Am Coll Cardiol. 2013; 62(16): 1401–1408.
  45. Sabatine MS, Giugliano RP, Keech AC, et al. FOURIER Steering Committee and Investigators. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017; 376(18): 1713–1722.
  46. Tomlinson B, Hu M, Zhang Y, et al. Alirocumab for the treatment of hypercholesterolemia. Expert Opin Biol Ther. 2017; 17(5): 633–643.
  47. Ibrahim NE, McCarthy CP, Shrestha S, et al. Effect of neprilysin inhibition on various natriuretic peptide assays. J Am Coll Cardiol. 2019; 73(11): 1273–1284.
  48. Chen S, Cao P, Dong N, et al. PCSK6-mediated corin activation is essential for normal blood pressure. Nat Med. 2015; 21(9): 1048–1053.
  49. Egom EE. BNP and heart failure: preclinical and clinical trial data. J Cardiovasc Transl Res. 2015; 8(3): 149–157.
  50. Korostyshevskaya IM, Maksimov VF, Rudenko NS. C-type natriuretic peptide: what, where and why? Neuro Behav Physiol. 2016; 46(8): 888–894.
  51. Rahbi H, Narayan H, Jones DJL, et al. The uroguanylin system and human disease. Clin Sci (Lond). 2012; 123(12): 659–668.
  52. Valentino MA, Lin JE, Snook AE, et al. A uroguanylin-GUCY2C endocrine axis regulates feeding in mice. J Clin Invest. 2011; 121(9): 3578–3588.
  53. Lorenz JN, Nieman M, Sabo J, et al. Uroguanylin knockout mice have increased blood pressure and impaired natriuretic response to enteral NaCl load. J Clin Invest. 2003; 112(8): 1244–1254.
  54. Miyazaki T, Otani K, Chiba A, et al. A new secretory peptide of natriuretic peptide family, osteocrin, suppresses the progression of congestive heart failure after myocardial infarction. Circ Res. 2018; 122(5): 742–751.
  55. Cui K, Huang W, Fan J, et al. Midregional pro-atrial natriuretic peptide is a superior biomarker to N-terminal pro-B-type natriuretic peptide in the diagnosis of heart failure patients with preserved ejection fraction. Medicine (Baltimore). 2018; 97(36): e12277.
  56. Czech M, Opolski G, Zdrojewski T, et al. The costs of heart failure in Poland from the public payer's perspective. Polish programme assessing diagnostic procedures, treatment and costs in patients with heart failure in randomly selected outpatient clinics and hospitals at different levels of care: POLKARD. Kardiol Pol. 2013; 71(3): 224–232.
  57. Mapa potrzeb zdrowotnych w zakresie kardiologii dla Polski. http://webcache.googleusercontent.com/search?q=cache:Om3bKiL7cEcJ:www.mz.gov.pl/wp-content/uploads/2015/12/MPZ_kardiologia_Polska.pdf+&cd=11&hl=en&ct=clnk&gl=pl (February 3, 2020).
  58. Maisel AS, Duran JM, Wettersten N. Natriuretic peptides in heart failure: atrial and B-type natriuretic peptides. Heart Fail Clin. 2018; 14(1): 13–25.
  59. Troughton RW, Richards AM, Yandle TG, et al. The effects of medications on circulating levels of cardiac natriuretic peptides. Ann Med. 2007; 39(4): 242–260.
  60. Ellinor PT, Low AF, Patton KK, et al. Discordant atrial natriuretic peptide and brain natriuretic peptide levels in lone atrial fibrillation. J Am Coll Cardiol. 2005; 45(1): 82–86.
  61. Baba M, Yoshida K, Ieda M. Clinical applications of natriuretic peptides in heart failure and atrial fibrillation. Int J Mol Sci. 2019; 20(11).
  62. Richards M, Di Somma S, Mueller C, et al. Atrial fibrillation impairs the diagnostic performance of cardiac natriuretic peptides in dyspneic patients: results from the BACH Study (Biomarkers in ACute Heart Failure). JACC Heart Fail. 2013; 1(3): 192–199.
  63. Knudsen CW, Omland T, Clopton P, et al. Impact of atrial fibrillation on the diagnostic performance of B-type natriuretic peptide concentration in dyspneic patients: an analysis from the breathing not properly multinational study. J Am Coll Cardiol. 2005; 46(5): 838–844.
  64. O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med. 2011; 365(1): 32–43.
  65. Sridharan S, Kini RM, Richards AM. Venom natriuretic peptides guide the design of heart failure therapeutics. Pharmacol Res. 2020; 155: 104687.
  66. Costello-Boerrigter LC, Schirger JA, Miller WL, et al. Cenderitide (CD-NP), a novel peptide designed to activate both guanylyl cyclase B and A, activates the second messenger cGMP, suppresses aldosterone, and preserves GFR without reducing blood pressure in a proof-of-concept study in patients with chronic heart failure. BMC Pharmacology. 2011; 11(S1).
  67. Cannone V, Cabassi A, Volpi R, et al. Jr. Atrial natriuretic peptide: a molecular target of novel therapeutic approaches to cardio-metabolic disease. Int J Mol Sci. 2019; 20(13).
  68. Packer M, O'Connor C, McMurray JJV, et al. TRUE-AHF Investigators. Effect of ularitide on cardiovascular mortality in acute heart failure. N Engl J Med. 2017; 376(20): 1956–1964.

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