Effect of Ramipril on Endothelin-1 Expression in Myocardial Tissue at Wistar Rats Induced Myocardial Infarction

Authors

  • Gestina Aliska Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Andalas, West Sumatra, Indonesia https://orcid.org/0000-0002-3234-898X
  • Yusticia Katar Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Andalas, West Sumatra, Indonesia
  • Liganda Endo Mahata Universitas Andalas
  • Nisa Pratiwi Medical Doctor Programme, Faculty of Medicine, Universitas Andalas, West Sumatra, Indonesia
  • Vinta Nuranisyah Medical Doctor Programme, Faculty of Medicine, Universitas Andalas, West Sumatra, Indonesia

DOI:

https://doi.org/10.3889/oamjms.2022.7676

Keywords:

ACE-Inhibitor, Endothelin-1, Myocardial infarction, Ramipril, Relative gene expression

Abstract

BACKGROUND: Acute myocardial infarction occurs due to a sudden decrease in coronary blood flow caused by coronary artery embolism, coronary dissection, or coronary vasospasm. The Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor; it is synthesized and released from vascular and endocardial endothelial cells and myocytes. The action of ET-1 induces endothelial dysfunction in the coronary circulation through several mechanisms, such as reduced NO pathway activity, increased oxidative stress and inflammation, and interference with glucose and lipid metabolism. Ramipril is one of the angiotensin-converting enzyme inhibitors (ACE-I) that can reduce the formation of ET-1 by enhancing the NO expression. NO can down-regulate the ET-1 secretion through soluble guanylate cyclase activation and increased cellular generation of cGMP.

AIM: This study aimed to investigate the effect of Ramipril on ET-1 expression in rats-induced myocardial infarction.

METHODS: Six-week-old male Wistar rats were randomly allocated into three groups: negative control, positive control was given NaCl 0.9% and treatment group treated with ramipril 3 mg/kg/day orally for 7 days. Myocardial infarction was induced in positive and treatment group by subcutaneous injection of isoproterenol, and 24 h after the last administration, rats were sacrificed to evaluate the relative expression of ET-1 using the real-time polymerase chain reaction and 2-ΔΔCt method.

RESULTS: The average expression for the negative control was 0.0098, positive control was 0.0136 and treatment group was 0.0118, with p = 0.210 (p > 0.05).

CONCLUSION: Our data suggest that there is no difference between groups for the relative expression of ET-1.

Downloads

Download data is not yet available.

Metrics

Metrics Loading ...

Plum Analytics Artifact Widget Block

References

Mechanic OJ. Acute myocardial infarction. In: StatPearls. Treasure Island, FL. StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459269/#!po=91.6667 [Last accessed on 2020 Apr 07].

Skovsted GF, Kruse LS, Berchtold LA, Grell AS, Warfvinge K, Edvinsson L. Myocardial ischemia-reperfusion enhances transcriptional expression of endothelin-1 and vasoconstrictor ETB receptors via the protein kinase MEK-ERK1/2 signaling pathway in rat. PLoS One. 2017;12(3):1-18. https://doi.org/10.1371/journal.pone.0174119 PMid:28323857 DOI: https://doi.org/10.1371/journal.pone.0174119

Kolettis TM, Barton M, Langleben D, Matsumura Y. Endothelin in coronary artery disease and myocardial infarction. Cardiol Rev. 2013;21(5):249-56. https://doi.org/10.1097/CRD.0b013e318283f65a PMid:23422018 DOI: https://doi.org/10.1097/CRD.0b013e318283f65a

Kelly LK, Wedgwood S, Steinhorn RH, Black SM. Nitric oxide decreases endothelin-1 secretion through the activation of soluble guanylate cyclase. Am J Physiol Lung Cell Mol Physiol. 2004;286(530-5):984-91. https://doi.org/10.1152/ajplung.00224.2003 PMid:14695117 DOI: https://doi.org/10.1152/ajplung.00224.2003

Pfeffer MA. ACE inhibitors in acute myocardial infarction: Patient selection and timing. Circulation. 1998;97(22):2192-4. https://doi.org/10.1161/01.cir.97.22.2192 PMid:9631866 DOI: https://doi.org/10.1161/01.CIR.97.22.2192

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut. 4th ed. Jakarta: Perhimpunan Dokter Spesialis Kardiovaskular Indonesia; 2018.

Herman LL, Bashir K. Angiotensin Converting Enzyme Inhibitors (ACEI). In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2019. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431051/#_NBK431051_pubdet [Last accessed on 2020 Apr 07].

Bayir Y, Cadirci E, Suleyman H, Halici Z, Keles MS. Effects of lacidipine, ramipril and valsartan on serum BNP levels in acute and chronic periods following isoproterenol-induced myocardial infarction in rats. Eurasian J Med. 2009;41(1):44-8. PMid:25610063

Mahboudi H, Heidari NM, Rashidabadi ZI, Anbarestani AH, Karimi S, Darestani KD. Prospect and Competence of Quantitative Methods via Real-time PCR in a Comparative Manner: An Experimental Review of Current Methods. Open Bioinform J 2018;11(1):1-11. http://doi.org/10.2174/1875036201811010001 DOI: https://doi.org/10.2174/1875036201811010001

Desideri G, Grassi D, Croce G, Bocale R, Tiberti S, Evangelista S, et al. Different effects of angiotensin-converting enzyme inhibitors on endothelin-1 and nitric oxide balance in human vascular endothelial cells: Evidence of an oxidant-sensitive pathway. Mediators Inflamm. 2008;2008:305087. https://doi.org/10.1155/2008/305087 PMid:19079593 DOI: https://doi.org/10.1155/2008/305087

Ancion A, Tridetti J, Trung MN. A review of the role of bradykinin and nitric oxide in the cardioprotective action of angiotensin-converting enzyme inhibitors : Focus on perindopril. Cardiol Ther. 2019;8(2):179-91. http://doi.org/10.1007/s40119-019-00150-w PMid:31578675 DOI: https://doi.org/10.1007/s40119-019-00150-w

Versari D, Daghini E, Virdis A, Ghiadoni L, Taddei S. Endothelial dysfunction as a target for prevention of cardiovascular disease. Diabetes Care. 2009;32(Suppl 2):S314-21. DOI: https://doi.org/10.2337/dc09-S330

Ová OP, Šimko F. The role of nitric oxide in the maintenance of vasoactive balance. Physiol Res. 2007;56(2):S7-16. http://doi.org/10.33549/physiolres.931392 PMid:17824812 DOI: https://doi.org/10.33549/physiolres.931392

Lobo R, Chandrasekhar Sagar B, Shenoy C. Bio-tea prevents membrane destabilization during Isoproterenol-induced myocardial injury. J Microsc Ultrastruct. 2016;5(3):146-54. http://doi.org/10.1016/j.jmau.2016.09.001 PMid:30023249 DOI: https://doi.org/10.1016/j.jmau.2016.09.001

Comini L, Bachetti T, Cargnoni A, Bastianon D, Gitti GL, Ceconi C, et al. Therapeutic modulation of the nitric oxide: All ace inhibitors are not equivalent. Pharmacol Res. 2007;56(1):42-8. http://doi.org/10.1016/j.phrs.2007.03.004 PMid:17475504 DOI: https://doi.org/10.1016/j.phrs.2007.03.004

de Snchez VC, Yañez-Maldonado L, Vidrio-Gómez S, Martínez L, Suárez J, Aranda-Fraustro A, et al. Role of nitric oxide in isoproterenol-induced myocardial infarction. In: Cardiotoxicity of Oncologic Treatments; 2012. https://doi.org/10.5772/34505 DOI: https://doi.org/10.5772/34505

Mohamed Saleem TS, Bharani K, Gauthaman K. ACE inhibitors-angiotensin II receptor antagonists: A useful combination therapy for ischemic heart disease. Open Access Emerg Med. 2010;2:51-9. http://doi.org/10.2147/oaem.s10507 PMid:27147838 DOI: https://doi.org/10.2147/OAEM.S10507

Keles MS, Bayir Y, Suleyman H, Halici Z. Investigation of effects of Lacidipine, Ramipril and Valsartan on DNA damage and oxidative stress occurred in acute and chronic periods following isoproterenol-induced myocardial infarct in rats. Mol Cell Biochem. 2009;328(1-2):109-17. http://doi.org/10.1007/s11010-009-0080-y PMid:19296206 DOI: https://doi.org/10.1007/s11010-009-0080-y

Rosiansky-Sultan M, Klipper E, Spanel-Borowski K, Meidan R. Inverse relationship between nitric oxide synthases and endothelin-1 synthesis in bovine corpus luteum: Interactions at the level of luteal endothelial cell. Endocrinology. 2006;147(11):5228-35. http://doi.org/10.1210/en.2006-0795 PMid:16887911 DOI: https://doi.org/10.1210/en.2006-0795

Sud N, Black SM. Endothelin-1 impairs nitric oxide signaling in endothelial cells through a protein kinase cδ-dependent activation of STAT3 and decreased endothelial nitric oxide synthase expression. DNA Cell Biol. 2009;28(11):543-53. http://doi.org/10.1089/dna.2009.0865 PMid:19754268 DOI: https://doi.org/10.1089/dna.2009.0865

Downloads

Published

2022-01-01

How to Cite

1.
Aliska G, Katar Y, Endo Mahata L, Pratiwi N, Nuranisyah V. Effect of Ramipril on Endothelin-1 Expression in Myocardial Tissue at Wistar Rats Induced Myocardial Infarction. Open Access Maced J Med Sci [Internet]. 2022 Jan. 1 [cited 2024 Mar. 19];10(A):33-7. Available from: https://oamjms.eu/index.php/mjms/article/view/7676

Funding data

Most read articles by the same author(s)