Association of N-Terminal Pro–Brain Natriuretic Peptide, Matrix –Metalloprotinase-9, and 8-Oxo-2 Deoxy Guanosine with the Incidence of Essential Hypertension
American Journal of Internal Medicine
Volume 3, Issue 2, March 2015, Pages: 67-77
Received: Mar. 8, 2015; Accepted: Mar. 19, 2015; Published: Mar. 23, 2015
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Authors
Julian Yonan Ismaeil, Ministry of Health, Aen Kawa, Erbil, Iraq
Shatha Rouf Moustafa, Clinical Analysis Department, College of Pharmacy, Hawler Medical University, Havalan city, Erbil, Iraq
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Abstract
Background and Objectives: Oxidative stress and inflammation are cooperative events involved in essential hypertension diseases. This study was as a step for elucidating the contribution of N-terminal pro-brain natriuretic peptide, matrix-metalloprotinase-9 and 8-oxo2-deoxyguanosine with the essential hypertension incidence, development, and progression. Aims: The objective was to determine the serum studied parameters levels in essential hypertensive and normotensive subjects, and to assess the association between these biomarkers with the essential hypertension, and to investigate the effect of other confounding factors like stages, age, and gender and finally find the correlation between all studied parameters. Methods: This study was designed to examine the associations between the focused parameters with the essential hypertension on 50 patients of both genders, as well as an equal numbers of matched age–gender healthy adults were also enrolled in this study as a control group. The hypothesis suggesting that oxidative stress and inflammatory processes influence the risk of adverse clinical outcomes are worth investigating. These parameters were analyzed using enzyme linked immunosorbent assay. Statistical analyses were performed with SPSS version 18. Results: Patients with essential hypertension exhibited significantly higher serum focused parameters levels as compared with the control group. The mean serum N-terminal pro–brain natriuretic peptide levels in patients and control groups were 304.33 ± 204.19, 76.52±20.98 pg/ml respectively. The mean serum matrix–metalloprotinase-9 level in patients and control groups were 2.36±1.1, 1.4±0.8 respectively. The mean serum 8-oxo-2-deoxy guanosine level in patients and control groups were 170.40±41.95, 84.11±34.07 (mg/ml) respectively. Conclusions: Data suggested an association between these circulating biomarkers with the incidence, development, and progression of essential hypertension. No effect of age and gender present on serum levels of focused biomarkers in both groups. These focused parameters seem to be a simple, non-invasive tools and independent parameters for early detection, assessing disease severity, and involved in the etiology of disease. Data indicated an alteration in the oxidative status and inflammatory processes in patients with essential hypertension. Accordingly, this work was undertaken to assess contribution of the oxidative stress and inflammatory process as a risk factors. In addition, these parameters are regarded as markers with prognostic significance and as potential therapeutic targets. These biomarkers are tools that might aid the physicians in diagnosis and subsequent risk stratification, guiding selection of therapy, secondary prevention, and serving as a target for therapy.
Keywords
Essential Hypertension, N-Terminal Pro-Brain Natriuretic Peptide, Matrix-Metalloprotinase-9, 8-Oxo2-Deoxyguanosine
To cite this article
Julian Yonan Ismaeil, Shatha Rouf Moustafa, Association of N-Terminal Pro–Brain Natriuretic Peptide, Matrix –Metalloprotinase-9, and 8-Oxo-2 Deoxy Guanosine with the Incidence of Essential Hypertension, American Journal of Internal Medicine. Vol. 3, No. 2, 2015, pp. 67-77. doi: 10.11648/j.ajim.20150302.14
References
[1]
Olsson LG, Swedberg K, Cleland JG, Spark PA, Komajda M, Metra M, Torp-Pedersen C, Remme WJ, Scherhag A, Poole-Wilson P. (2007). Prognostic importance of plasma NT-pro BNP in chronic heart failure in patients treated with a beta-blocker: results from the Carvedilol Or Metoprolol European Trial (COMET) trial. Eur J Heart Fail, 9 :795- 801.
[2]
Lainchbury JG, Troughton RW, Strangman KM, Frampton CM, Pilbrow A, Yandle TG, Hamid AK, Nicholls MG, Richards AM. (2010). N-terminal pro-B-type natriuretic peptide-guided treatment for chronic heart failure: results from the battlescarred (NT-proBNP-Assisted Treatment To Lessen Serial Cardiac Readmissions and Death) trial. J Am Coll Cardiol, 55:53-60.
[3]
Lee YH, Kim TY, Hong YM. (2009). Metalloproteinase-3 genotype as a predictor of cardiovascular risk in hypertensive adolescents. Korean circulation journal, 39 (8): 328- 334.
[4]
Murray DB, Levick SP, Brower GL, Janicki JS. (2010). Inhibition of matrix metal-loproteinase activity prevents increases in myocardial tumor necrosis factor-alpha. J Mol Cell Cardiol, 49: 245– 250.
[5]
Benjamin MM, Khalil RA. (2012). Matrix metalloproteinase inhibitors as investigative tools in the pathogenesis and management of vascular disease. EXS, 103:209– 279.
[6]
Fingleton B. (2007). Matrix metalloproteinases as valid clinical targets. Curr pharm Des, 13 (3): 333- 346.
[7]
Ogita H, Liao J. (2004). Endothelial function and oxidative stress. Endothelium, 11: 123- 132.
[8]
Delaney S, Jarem DA, Volle CB, Yennie CJ. (2012). Chemical and biological consequences of oxidatively damaged guanine in DNA. Free Radic Res, 46 (4): 420- 441.
[9]
Patra A, Nagy LD, Zhang Q, Su Y, Müller L, Guengerich FP, Egli M. (2014). Kinetics, Structure, and Mechanism of 8-Oxo-7,8-dihydro-2'-deoxyguanosine Bypass by Human DNA Polymerase. J Biol Chem.2014; doi: 10.1074/jbc.M114.551820.
[10]
Vivek Thakkar, Wendy M Stevens, David Prior, Owen A Moore, Jillian Byron, Danny Liew, Karen Patterson, Pravin Hissaria, Janet Roddy, Jane Zochling, Joanne Sahhar, Peter Nash, Kathleen Tymms, David Celermajer, Eli Gabbay, Peter Youssef, Susanna M Proudman and Mandana Nikpour, (2012). N-terminal pro-brain natriuretic peptide in a novel screening algorithm for pulmonary arterial hypertension in systemic sclerosis: a case-control study. Arthritis Research & Therapy, 114: 143.
[11]
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, (1997). The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). Arch Intern Med, 157 :2413– 2446.
[12]
Olsen MH, Wachtell K, Tuxen C, Fossum E, Bang LE, Hall C, Ibsen H,Rokkedal J, Devereux RB, Hildebrandt P. (2004). N-terminal pro-brain natriuretic peptide predicts cardiovascular events in patients with hypertension and left ventricular hypertrophy: a LIFE study. J Hypertens, 22: 1597– 1600.
[13]
Pedersen F, Raymond I, Kistorp C, Sandgaard N, Jacobsen P, Hildebrandt P. (2005). N-terminal pro-brain natriuretic peptide in arterial hypertension: a valuable prognostic marker of cardiovascular events. J Card Fail, 11: 70 – 75.
[14]
Olsen MH, Wachtell K, Nielsen OW, Hall C, Wergeland R, Ibsen H, Kjeldsen SE, Devereux RB, Dahlof B, Hildebrandt PR. (2006). N-terminal brain natriuretic peptide predicted cardiovascular events stronger than highsensitivity C-reactive protein in hypertension: a LIFE substudy. J Hypertens, 24:1531– 1539.
[15]
Vinciane Paget, Liliana Legedz, Nathalie Gaudebout, Nicolas Girerd, Giampiero Bricca, Hugues Milon,Madeleine Vincent, Pierre Lantelme, (2011). N-Terminal Pro-Brain Natriuretic Peptide A Powerful Predictor of Mortality in Hypertension. Hypertension, 57: 702- 709.
[16]
Per Hildebrandt, Mikael Boesen, Michael Olsen, Kristian Wachtell and Bjoern Groenning, (2004). N-terminal pro brain natriuretic peptide in arterial hypertension—a marker for left ventricular dimensions and prognosis. Eur J Heart Fail, 6 (3): 313 - 317.
[17]
Kenan İltümür, Aziz Karabulut, Nizamettin Topreak, (2005). NT-proBNP in Isolated Diastolic Dysfunction. Dicle Tıp Dergisi, 32 (4): 165- 171.
[18]
Mueller T, Gegenhuber A, Dieplinger B, Poelz W, Haltmayer M.(2005) . Capacity of B-type natriuretic peptide (BNP) and amino-terminal proBNP as indicators of cardiac structural disease in asymptomatic patients with systemic arterial hypertension. Clin Chem, 51: 2245 - 2251.
[19]
Halse KG, Lindegaard MLS, Goetze JP, Damm P, Mathiesen ER, Nielsen LB. (2005). Increased pro-B-type natriuretic peptide in infants of women with type I diabetes. Clin Chem, 51: 2296- 2302.
[20]
Conen D, Zeller A, Pfisterer M, Martina B. (2006). Usefulness of B-type natriuretic peptide and C-reactive protein in predicting the presence or absence of left ventricular hypertrophy in patients with systemic hypertension. Am J Cardiol, 97: 249 – 252.
[21]
Belluardo P, Cataliotti A, Bonaiuto L, Giuffre E, Maugeri E, Noto P,Orlando G, Raspa G, Piazza B, Babuin L, Chen HH, Martin FL, McKie PM, Heublein DM, Burnett JC Jr, Malatino LS. (2006). Lack of activation of molecular forms of the BNP system in human grade 1 hypertension and relationship to cardiac hypertrophy. Am J Physiol Heart Circ Physiol, 291: 1529 – 1535.
[22]
Mouly-Bertin C, Bissery A, Milon H, Dzudie A, Rabilloud M, Bricca G,Vincent M, Lantelme P. (2008). N-terminal pro-brain natriuretic peptide: a promising biomarker for the diagnosis of left ventricular hypertrophy in hypertensive women. Arch Cardiovasc Dis, 101:307– 315.
[23]
Morillas P, Castillo J, Quiles J, Nunez D, Guillen S, Maceira A, Rivera M, Bertomeu V. (2008). Usefulness of NT-proBNP level for diagnosing leftventricular hypertrophy in hypertensive patients: a cardiac magnetic resonance study. Rev Esp Cardiol, 61:972– 975.
[24]
Toda K, Sato Y, Hara T, Hijiya K, Kaneko R, Okada T, Takatsu Y, Fujiwara H, Iwasaki T. (2010). Correlates of NT-proBNP concentration in patients with essential hypertension in absence of congestive heart failure. J Clin Lab Anal, 24 (1):12- 6.
[25]
Giampiero Bricca, Pierre Lantelme, (2011). Natriuretic peptides: Ready for prime-time in hypertension? Elsevier, 104 ( 6–7): 403– 409.
[26]
Paget V, Legedz L, Gaudebout N, Girerd N, Bricca G, Milon H. (2011). N-terminal pro-brain natriuretic peptide. A powerful predictor of mortality in hypertension. Hypertension, 57:702- 709.
[27]
Alexis E. Malavazos1, Lelio Morricone1, Alessandro Marocchi, Federica Ermetici1, Bruno Ambrosi and Massimiliano M. Corsi, (2006). N-Terminal Pro-B-Type Natriuretic Peptide and Echocardiographic Abnormalities in Severely Obese Patients: Correlation with Visceral Fat .Clinical Chemistry, 52 (6): 1211- 1213.
[28]
Mueller T, Gegenhuber A, Poelz W, Haltmayer M. (2004). Head-to-head comparison of the diagnostic utility of BNP and NT-proBNP in symptomatic and asymptomatic structural heart disease. Clin Chim Acta, 341: 41– 48.
[29]
Tschope C, Kasner M, Westermann D. (2005). The role of NT-proBNP in the diagnostics of isolated diastolic dysfunction: correlation with echocardiographic and invasive measurements. Eur Heart J, 26:2277.
[30]
Bautista LE. (2003). Inflammation, endothelial dysfunction, and the risk of high blood pressure: epidemiologic and biological evidence. J HumHypertens, 17: 223- 230.
[31]
Zhou S, Feely J, Spiers JP, Mahmud A. (2007). Matrix metalloproteinase-9 polymorphism contributes to blood pressure and arterial stiffness in essential hypertension. J Hum Hypertens, 7 (21): 861– 867.
[32]
Boos CJ, Lip GY. (2006). Is hypertension an inflammatory process? Curr Pharm Des, 12:1623– 1635.
[33]
Raffetto JD, Khalil RA. (2008). Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease. Biochem Pharmacol, 75:346 – 359.
[34]
Derosa G, D'Angelo A, Ciccarelli L. (2006). Matrix Metalloproteinase-2, -9, and Tissue Inhibitor of Metalloproteinase-1 in Patients with Hypertension. Endothelium, 13: 227– 231.
[35]
Tan J, Hua Q, Xing X,Wen J, Liu R, Yang Z. (2007). Impact of the metalloproteinase-9/tissue inhibitor of metalloproteinase-1 system on large arterial stiffness in patients with essential hypertension. Hypertens Res, 30: 959– 963.
[36]
Ryan S, Frise,Fangwen Rao and Daniel TO, Connor, (2009). Matrix Metalloproteinases: Discrete Elevations in Essential Hypertension and Hypertensive End-Stage Renal Disease. Clinical and experimental hypertension, 31 (7): 521- 533.
[37]
Berg G, Miksztowicz V, Schreier L. (2011). Metalloproteinases in metabolic syndrome. Clinica Chimica Acta, 412 :1731 - 1739.
[38]
Tomohiro Kurihara, Ryoko Shimizu-Hirota, MD, Masayuki Shimoda, Takeshi Adachi, Hideyuki Shimizu, Stephen J. Weiss, Hiroshi Itoh, Shingo Hori, Naoki Aikawa, Yasunori Okada, (2012). Neutrophil-Derived Matrix Metalloproteinase 9 Triggers Acute Aortic Dissection. Circulation, 126: 3070- 3080.
[39]
Li YY, McTiernan CF, Feldman AM. (2000). Interplay of matrix metalloproteinases, tissue inhibitors of metalloproteinases and their regulators in cardiac matrix remodeling. Cardiovasc Res, 46: 214– 224.
[40]
Zervoudaki A, Economou E, Pitsavos C, Vasiliadou K, Aggeli C, Tsioufis K, Toutouza M, Stefanadis C, Toutouzas P. (2004). The effect of Ca2+ channel antagonists on plasma concentrations of matrix metalloproteinase-2 and -9 in essential hypertension. Am J Hypertens, 7: 273– 276.
[41]
Ahmed SH, Clark LL, Pennington WR, Webb CS, Bonnema DD, Leonardi AH, McClure CD, Spinale FG, Zile MR. (2006). Matrix metalloproteinases/tissue inhibitors of metalloproteinases: Relationship between changes in proteolytic determinants of matrix composition and structural, functional, and clinical manifestations of hypertensive heart disease. Circulation, 113:2089– 2096.
[42]
Josep Redón, Maria R, Oliva, Carmen Tormos, Vicente Giner, Javier Chaves, Antonio Iradi, Guillermo T. Sáez, (2003). Antioxidant Activities and Oxidative Stress Byproducts in Human Hypertension. Hypertension, 41: 1096- 1001.
[43]
Espinosa O, Jimenez-Almazan J, Chaves F J, Tormos M C, Clapes S, Iradi A, Salvador A, Fandos M, Redón J, Sáez G T.(2007). Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine(8-oxo-dG), a reliable oxidative stress marker in hypertension. Free Radic. Res, 41:546– 554.
[44]
Ferri, J, Martinez-Hervas S, Espinosa O, Fandos M, Pedro T, Real JT, Chaves F J, Cerdá C, Sáez G, Ascaso J F. (2008). 8-oxo-7,8-dihydro-2'-deoxyguanosine as a marker of DNA oxidative stress in individuals with combined familiar hyperlipidemia . Med. Clin. (Barc.), 131:1–4.
[45]
Maria L, Mansego, Josep Redon, Sergio Martinez-Hervas,Jose T Real, Fernando Martinez, Sebastian Blesa,Veronica Gonzalez-Albert, Guillermo T Saez, Rafael Carmena, Felipe J, Chaves, (2011). Different Impacts of Cardiovascular Risk Factors on Oxidative Stress. Int. J. Mol. Sci, 12: 6146- 6163.
[46]
Subash P, Gurumurthy P, Sarasabharathi A, Cherian K M. (2010). Urinary 8-OHdG: A Marker of Oxidative Stress to DNA and Total Antioxidant Status in Essential Hypertension with South Indian Population. Indian Journal of Clinical Biochemistry, 25 (2):127- 132.
[47]
Mussalo H, Vanninen E, Hartikainen J. (2003). NT-proANP and BNP in renovascular and in severe and mild essentila hypertension. Kidney Blood Press R, 26:34-41.
[48]
Pfister R, Tan D, Thekkanal J, Erdmann E, Schneider CA. (2008). Predictive value of NT-pro-BNP for the non-cardiologist. A study on 573 hospitalized patients with cardiovascular disease. Dtsch Med Wochenschr, 133 (12): 564 - 569.
[49]
Schöneich C. (1999). Reactive oxygen species and biological aging: a mechanistic approach. Exp Gerontol, 34: 19-34.
[50]
Das SK, Sanyal K, Basu A. (2005). Study of urban community survey in India: Growing trend of high prevalence in developing country. Int J Med Sci, 2:70- 78.
[51]
Busserolles J, Mazur A, Gueux E, Rock E, Rayssiguier Y.(2002). Metabolic syndrome in the rat: Females are protected against the pro-oxidant effect of a high sucrose diet. Exp Biol Med, 227: 837- 842.
[52]
Torres-Ramalho, Paulo; Araújo, José Paulo; Bettencourt, Paulo; Moura, Luís M. (2012). Natriuretic peptides in aortic stenosis.Rev Port Cardiol, 31:655- 660.
[53]
Wang TJ, Larson MG, Levy D, Leip EP, Benjamin EJ, Wilson PW, Sutherland P, Omland T, Vasan RS. (2002). Impact of age and sex on plasma natriuretic peptide levels in healthy adults. Am J Cardiol, 90: 254 - 558.
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