Current issue
About the Journal
Scientific Council
Editorial Board
Regulatory and archival policy
Code of publishing ethics
Publisher
Information about the processing of personal data in relation to cookies and newsletter subscription
Archive
For Authors
For Reviewers
Contact
Reviewers
Annals reviewers in 2023
Annals reviewers in 2022
Annals reviewers in 2021
Annals reviewers in 2020
Annals reviewers in 2019
Annals reviewers in 2018
Annals reviewers in 2017
Annals reviewers in 2016
Annals reviewers in 2015
Annals reviewers in 2014
Annals reviewers in 2013
Annals reviewers in 2012
Links
Sklep Wydawnictwa SUM
Biblioteka Główna SUM
Śląski Uniwersytet Medyczny w Katowicach
Privacy policy
Accessibility statement
Reviewers
Annals reviewers in 2023
Annals reviewers in 2022
Annals reviewers in 2021
Annals reviewers in 2020
Annals reviewers in 2019
Annals reviewers in 2018
Annals reviewers in 2017
Annals reviewers in 2016
Annals reviewers in 2015
Annals reviewers in 2014
Annals reviewers in 2013
Annals reviewers in 2012
Age-related alterations in arginase-NO-synthase system in patients with coronary heart disease associated with hypertension
1
Department of family medicine FPGE, Lviv National Medical University of Ukraine
Corresponding author
Anna Besedina
Department of family medicine FPGE, Lviv National Medical University of Ukraine, 79059, Liviv Emergency Hospital (KMK LSHMD), Mykolaychuka 9, Liviv, Ukraine
Department of family medicine FPGE, Lviv National Medical University of Ukraine, 79059, Liviv Emergency Hospital (KMK LSHMD), Mykolaychuka 9, Liviv, Ukraine
Ann. Acad. Med. Siles. 2016;70:40-45
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Coronary heart disease (CHD) is the most common heart diseases in Europe. The aim of this study was to determine the intensity of L-arginine metabolism by two alternative pathways (oxidative by NOS and nonoxid-ative by arginase) in the blood plasma of patients with CHD associated with hypertension (HT) of different age groups.
Materials and methods:
50 patients with isolated CHD and 42 patients with CHD associated with HT were enrolled in this study. NOS activity was determined by nitrite anion formed in the reaction. Arginase activity was tested by the formation of urea.
Results:
In middle-aged patients with isolated CHD, the total NOS activity statistically significantly increased by 2.2 fold in comparison with healthy subjects of the same age group. In patients with CHD associated with HT, the total NOS activity statistically significantly increased in both middle-aged and older persons 2.3-fold than in healthy subjects of the same age groups. In patients with isolated CHD, the arginase activity increases 1.5-fold in middle-aged patients and 1.7-fold in older patients compared with the healthy participants. In the middle-aged and older patients with CHD associated with HT, the arginase activity statistically significantly increased 1.7- and 1.8-fold than in the healthy subjects of the same age groups.
Conclusions:
In patients with isolated CHD and patients with CHD associated with HT, an increased total NO-synthase and arginase activity in comparison with healthy individuals was found. It was shown that the increase in NO-synthase and arginase activity is more expressed in older patients than middle-aged patients.
Coronary heart disease (CHD) is the most common heart diseases in Europe. The aim of this study was to determine the intensity of L-arginine metabolism by two alternative pathways (oxidative by NOS and nonoxid-ative by arginase) in the blood plasma of patients with CHD associated with hypertension (HT) of different age groups.
Materials and methods:
50 patients with isolated CHD and 42 patients with CHD associated with HT were enrolled in this study. NOS activity was determined by nitrite anion formed in the reaction. Arginase activity was tested by the formation of urea.
Results:
In middle-aged patients with isolated CHD, the total NOS activity statistically significantly increased by 2.2 fold in comparison with healthy subjects of the same age group. In patients with CHD associated with HT, the total NOS activity statistically significantly increased in both middle-aged and older persons 2.3-fold than in healthy subjects of the same age groups. In patients with isolated CHD, the arginase activity increases 1.5-fold in middle-aged patients and 1.7-fold in older patients compared with the healthy participants. In the middle-aged and older patients with CHD associated with HT, the arginase activity statistically significantly increased 1.7- and 1.8-fold than in the healthy subjects of the same age groups.
Conclusions:
In patients with isolated CHD and patients with CHD associated with HT, an increased total NO-synthase and arginase activity in comparison with healthy individuals was found. It was shown that the increase in NO-synthase and arginase activity is more expressed in older patients than middle-aged patients.
REFERENCES (31)
1.
Reid C.M., Owen A.J., Freedman B. Coronary artery disease epidemics: not all the same. Medicographia. 2014; 36(1): 11–18.
2.
Padial L.R. Optimizing secondary prevention treatment in stable coronary artery disease. Medicographia. 2009; 31(4): 384–391.
3.
Rosendorff C., Black H., Cannon C., Gorsh B.J., Gore J., Izzo J.L.Jr., Kaplan N.M., O’Connor C.M., O’Gara P.T., Oparil S. Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention. Circulation 2007; 115: 2761–2788.
4.
Dudzinski D.M., Igarashi J., Greif D., Michel T. The regulation and pharmacology of endothelial nitric oxide synthase. Annu. Rev. Pharmacol. Toxicol. 2006; 46: 235–276.
5.
Félétou M., Vanhoutte P.M. Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture). Am. J. Physiol. Heart Circ. Physiol. 2006; 291: H985–H1002.
6.
Syed R., Biyabani M.U., Prasad S., Deeba F., Jamil K. Correlation and identification of variable number of tandem repeats of eNOS gene in coronary artery disease. Saudi J. Biol. Scien. 2010; 17(3): 209–213.
7.
Ming X.F., Barandier C., Viswambharan H., Kwak B.R., Mach F., Mazzolai L., Hayoz D., Ruffieux J., Rusconi S., Montani J.P., Yang Z. Thrombin stimulates human endothelial arginase enzymatic activity via RhoA/ROCK pathway: implications for atherosclerotic endothelial dysfunction. Circulation 2004; 110: 3708–3714.
8.
Bachetti T., Comini L., Francolini G., Bastianon D., Valetti B., Cadei M., Grigolato P., Suzuki H., Finazzi D., Albertini A., Curello S., Ferrari R. Arginase pathway in human endothelial cells in pathophysiological conditions. J. Mol. Cell. Cardiol. 2004; 37: 515–523.
9.
Berkowitz D.E., White R., Li D., Minhas K.M., Cernetich A., Kim S., Burke S., Shoukas A.A., Nyhan D., Champion H.C., Hare J.M. Arginase reciprocally regulates nitric oxide synthase activity and contributes to endothelial dysfunction in aging blood vessels. Circulation 2003; 108(16): 2000–2006.
10.
Hein T.W., Zhang C., Wang W., Chang C.I., Thengchaisri N., Kuo L. Ischemia-reperfusion selectively impairs nitric oxide-mediated dilation in coronary arterioles: counteracting role of arginase. FASEB J. 2003; 17: 2328–2330.
11.
Guevara I., Iwanejko J., Dembińska-Kieć A., Pankiewicz J., Wanat A., Anna P., Gołabek I., Bartuś S., Malczewska-Malec M., Szczudlik A. Determination of nitrite/nitrate in human biological material by the simple Griess reaction. Clin. Chim. Acta 1998; 274: 177–188.
12.
Umar S., Van der Laarse A. Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart. Mol. Cell. Biochem. 2010; 333(1–2): 191–201.
13.
Akizuki E., Akaike T., Okamoto S., Fujii S., Yamaguchi Y., Ogawa M., Maeda H. Role of NO and superoxide in acute cardiac allograft rejection in rats. Proc. Soc. Exp. Biol. Med. 2000; 225(2): 151–159.
14.
Gawad S., Yossof M., Soliman A., Abd El-Aziz A.A., El-Shahat F.B., Selim A.K. Expression of inducible nitric oxide synthase gene in diabetic and non-diabetic coronary artery disease patients. Researcher 2011; 3(6): 40–48.
15.
Ferreiro C.R., Chagas A.C., Carvalho M.H., Dantas A.P., Scavone C., Souza L.C., Buffolo E., da Luz P.L. Expression of inducible nitric oxide synthase is increased in patients with heart failure due to ischemic disease. Braz. J. Med. Biol. Res. 2004; 37: 1313–1320.
16.
Santhanam L., Lim H.K., Lim H.K., Miriel V., Brown T., Patel M., Balanson S., Ryoo S., Anderson M., Irani K., Khanday F., DiCostanzo L., Nyhan D., Hare J.M., Christianson D.W., Rivers R., Shoukas A., Berkowitz D.E. Inducible NO synthase dependent S-nitrosylation and activation of arginase 1 contribute to age – related endothelial dysfunction. Circ. Res. 2007; 101: 692–702.
17.
Cuzzocrea S., Mazzon E., Dugo L., Di Paola R., Caputi A.P., Salvemini D. Superoxide: a key player in hypertension. FASEB J. 2004; 18: 94–101.
18.
Lubos E., Handy D.E., Loscalzo J. Role of oxidative stress and nitric oxide in atherothrombosis. Front. Biosci. 2008; 13: 5323–5344.
19.
Cook S. Coronary artery disease, nitric oxide and oxidative stress: the "Yin-Yang" effect – a Chinese concept for a worldwide pandemic. Swiss Med. Wkly. 2006; 136: 103–113.
20.
Lee C.Y., Yen M.H. Nitric oxide and carbon monoxide, collaborative and competitive regulators of hypertension. Chang Gung Med. J. 2009; 32(1): 12–21.
21.
Mori M. Regulation of nitric oxide synthesis and apoptosis by arginase and arginine recycling. J. Nutr. 2007; 137(6 Suppl 2): 1616S–1620S.
22.
Morris S.M. Recent advances in arginine metabolism: roles and regulation of the arginases. Brit. J. Pharmacol. 2009; 157: 922–930.
23.
Durante W., Johnson F.K., Johnson R.A. A critical regulator of nitric oxide synthesis and vascular function. Clin. Exp. Pharmacol. Physiol. 2007; 34: 906–911.
24.
Mielczarek-Puta M., Chrzanowska A., Graboń W., Barańczyk-Kuźma A. New insights into arginase. Part II. Role in physiology and pathology. Postepy Hig. Med. Dosw. 2008; 62: 214–221.
25.
Li H., Meininger C.J., Hawker J.R.Jr., Haynes T.E., Kepka-Lenhart D., Mistry S.K., Morris S.M.Jr., Wu G. Regulatory role of arginase I and II in nitric oxide, polyamine, and proline syntheses in endothelial cells. Am. J. Physiol. Endocrinol. Metab. 2001; 280(1): E75–E82.
26.
Santhanam L., Christianson L. Nyhan D., Berkowitz D.E. Arginase and vascular aging. J. Appl. Physio. 2008; 105: 1632–1642.
27.
Berkowitz D.E. Arginase inhibition restores NOS coupling and reverses endothelial dysfunction and vascular stiffness in old rats. J. Appl. Physiol. 2009; 107: 1249–1357.
28.
White A.R., Ryoo S., Li D., Champion H.C., Steppan J., Wang D., Nyhan D., Shoukas A.A., Hare J.M., Berkowitz D.E. Knockdown of arginase I restores NO signaling in the vasculature of old rats. Hypertension 2006; 47(2): 245–251.
29.
Pernow J., Jung C. Arginase as a potential target in the treatment of cardiovascular disease: Reversal of arginine steal? Cardiovasc. Res. 2013; 98(3): 334–343.
30.
Ryoo S., Gupta G., Benjo A., Lim H.K., Camara A., Sikka G., Lim H.K., Sohi J., Santhanam L., Soucy K., Tuolay E., Baraban E., Ilies M., Gerstenblith G., Nyhan D., Shoukas A., Christianson D.W., Alp N.J., Champion H.C., Huso D., Berkowitz D.E. Endothelial arginase II: a novel target for the treatment of atherosclerosis. Circ. Res. 2008; 102(8): 923–932.
31.
Shemyakin A., Kövamees O., Rafnsson A. Arginase inhibition improves endothelial function in patients with coronary artery disease and type 2 diabetes mellitus. Circulation 2012; 126(25): 2943–2950.
Share
RELATED ARTICLE
| eISSN: | 1734-025X |
The Medical University of Silesia in Katowice, as the Operator of the annales.sum.edu.pl website, processes personal data collected when visiting the website. The function of obtaining information about Users and their behavior is carried out by voluntarily entered information in forms, saving cookies in end devices, as well as by collecting web server logs, which are in the possession of the website Operator. Data, including cookies, are used to provide services in accordance with the Privacy policy.
You can consent to the processing of data for these purposes, refuse consent or access more detailed information.
You can consent to the processing of data for these purposes, refuse consent or access more detailed information.
