The cardiovascular system's Renin-Angiotensin-Aldosterone System (RAAS).

  • Lamiaa Saoud Abbod Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq
  • Fatima Amir Abd Algabar Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq
Keywords: Renin-Angiotensin-aldosterone System (RAAS), Hypertension, Atherosclerosis, Vascular remodeling, CVD

Abstract

The renin-angiotensin-aldosterone system (RAAS) has a noteworthy part in triggering, and inflammation is maintained by its physiological agents. A crucial mechanism for the initiation and headway of CVD, including Hypertension and atherosclerosis, is inflammation. In addition to its primary function in controlling blood pressure and its contribution to Hypertension, RAAS has pro-inflammatory and profibrotic cellular and molecular effects. Cardiovascular and renal disorders can be treated more effectively by hindering RAAS. Proof recommends that RAAS inhibition enhances vascular remodelling and gets better CVD sequels. Lower levels of oxidative stress and endothelial dysfunction, vascular inflammation, and favourable effects on endothelial progenitor cell regeneration are likely the causes of RAAS inhibition's sound vascular effects.

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Author Biographies

Lamiaa Saoud Abbod, Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq

Technical Demonstrator, Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq

Fatima Amir Abd Algabar, Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq

Technical Demonstrator, Department of Nursing Technologies, Baquba Technical Institute, Middle Technical University, Diyala, Iraq

References

Ferrario CM, Strawn WB. Role of the renin-angiotensin-aldosterone system and proinflammatory mediators in cardiovascular disease. Am J Cardiol. 2006; 98(1):121-8.

DOI: https://doi.org/10.1016/j.amjcard.2006.01.059

Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension: The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. 1934; 59(3):347-79.

DOI: https://doi.org/10.1084/jem.59.3.347

Fyhrquist F, Saijonmaa O. Renin‐angiotensin system revisited. J Inter Med. 2008; 264(3):224-36.

DOI: https://doi.org/10.1111/j.1365-2796.2008.01981.x

Nguyen G, Delarue F, Burcklé C, Bouzhir L, Giller T, Sraer JD. Pivotal role of the renin/prorenin receptor in angiotensin II production and cellular responses to renin. J Clin Investig. 2002; 109(11):1417-27.

DOI: https://doi.org/10.1172/JCI14276.

Huang Y, Noble NA, Zhang J, Xu C, Border WA. Renin-stimulated TGF-β1 expression is regulated by a mitogen-activated protein kinase in mesangial cells. Kidney Int. 2007; 72(1):45-52.

DOI: https://doi.org/10.1038/sj.ki.5002243

Staessen JA, Li Y, Richart T. Oral renin inhibitors. Lancet. 2006; 368(9545):1449-56.

DOI: https://doi.org/10.1016/S0140-6736(06)69442-7

Gebru Y, Diao TY, Pan H, Mukwaya E, Zhang Y. Potential of RAS inhibition to improve metabolic bone disorders. BioMed Res Int. 2013.

DOI: https://doi.org/10.1155/2013/932691

Cannavo A, Bencivenga L, Liccardo D, Elia A, Marzano F, Gambino G, et al. Aldosterone and mineralocorticoid receptor system in cardiovascular physiology and pathophysiology. Oxid Med Cell Longev. 2018.

DOI: https://doi.org/10.1155/2018/1204598

Gustafsson F, Azizi M, Bauersachs J, Jaisser F, Rossignol P. Targeting the aldosterone pathway in cardiovascular disease. Fundam Clin Pharmacol. 2012; 26(1):135-45.

DOI: https://doi.org/10.1111/j.1472-8206.2011.01004.x

Donoghue M, Hsieh F, Baronas E, Godbout K, Gosselin M, Stagliano N, et al. A novel angiotensin-converting enzyme–related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Circ Res. 2000; 87(5):e1-9.

DOI: https://doi.org/10.1161/01.RES.87.5.e1

Zhong J, Guo D, Chen CB, Wang W, Schuster M, Loibner H, et al. Prevention of angiotensin II–mediated renal oxidative stress, inflammation, and fibrosis by angiotensin-converting enzyme 2. Hypertension. 2011; 57(2):314-22.

DOI: https://doi.org/10.1161/HYPERTENSIONAHA.110.164244

Ferrario CM. Angiotensin-converting enzyme 2 and angiotensin-(1-7) an evolving story in cardiovascular regulation. Hypertension. 2006; 47(3):515-21.

DOI: https://doi.org/10.1161/01.HYP.0000196268.08909.fb

Richard V, Hurel-Merle S, Scalbert E, Ferry G, Lallemand F, Bessou JP, et al. Functional evidence for a role of vascular chymase in the production of angiotensin II in isolated human arteries. Circulation. 2001; 104(7):750-2.

DOI: https://doi.org/10.1161/hc3201.094971

Tracy RP. Inflammation in cardiovascular disease: cart, horse, or both?. Circulation. 1998; 97(20):2000-2.

DOI: https://doi.org/10.1161/01.CIR.97.20.2000

Mason RP. Optimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomil. Vasc Health Risk Manag. 2011; 24:405-16.

DOI: https://doi.org/10.2147/VHRM.S20737

Parameswaran N, Patial S. Tumor necrosis factor-α signaling in macrophages. Crit Rev Eukaryot Gene Expr. 2010; 20(2).

DOI: https://doi.org/10.1615/CritRevEukarGeneExpr.v20.i2.10

Gao X, Belmadani S, Picchi A, Xu X, Potter BJ, Tewari-Singh N. Tumor necrosis factor-α induces endothelial dysfunction in Leprdb mice. Circulation. 2007; 115(2):245-54.

DOI: https://doi.org/10.1161/CIRCULATIONAHA.106.650671

Pelisek J, Rudelius M, Zepper P, Poppert H, Reeps C, Schuster T, et al. Multiple biological predictors for vulnerable carotid lesions. Cerebrovasc. Dis. 2009; 28(6):601-10.

DOI: https://doi.org/10.1159/000247605

Russo G, Leopold JA, Loscalzo J. Vasoactive substances: nitric oxide and endothelial dysfunction in atherosclerosis. Vasc Pharmacol. 2002; 38(5):259-69.

DOI: https://doi.org/10.1016/S1537-1891(02)00250-1

Zimmerman MA, Selzman CH, Reznikov LL, Miller SA, Raeburn CD, Emmick J, et al. Lack of TNF-α attenuates intimal hyperplasia after mouse carotid artery injury. Am J Physiol Regul Integr. 2002; 283(2):R505-12.

DOI: https://doi.org/10.1152/ajpregu.00033.2002

Fujita M, Shannon JM, Irvin CG, Fagan KA, Cool C, Augustin A, et al. Overexpression of tumor necrosis factor-α produces an increase in lung volumes and pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol . 2001; 280(1):L39-49.

DOI: https://doi.org/10.1152/ajplung.2001.280.1.L39

Lambert CM, Roy M, Meloche J, Robitaille GA, Agharazii M, Richard DE, et al. Tumor necrosis factor inhibitors as novel therapeutic tools for vascular remodeling diseases. Am J Physiol Lung Cell Mol Physiol . 2010; 299(4):H995-1001.

DOI: https://doi.org/10.1152/ajpheart.00562.2010

Krasinski K, Spyridopoulos I, Kearney M, Losordo DW. In vivo blockade of tumor necrosis factor-α accelerates functional endothelial recovery after balloon angioplasty. Circulation. 2001; 104(15):1754-6.

DOI: https://doi.org/10.1161/hc4001.098046

Han Y, Runge MS, Brasier AR. Angiotensin II induces interleukin-6 transcription in vascular smooth muscle cells through pleiotropic activation of nuclear factor-κB transcription factors. Circ Res. 1999; 84(6):695-703.

DOI: https://doi.org/10.1161/01.RES.84.6.695

Von Känel R, Mills PJ, Mausbach BT, Dimsdale JE, Patterson TL, Ziegler MG, et al. Effect of Alzheimer caregiving on circulating levels of C-reactive protein and other biomarkers relevant to cardiovascular disease risk: a longitudinal study. Gerontol. 2012; 58(4):354-65.

DOI: https://doi.org/10.1159/000334219

Hurlimann J, Thorbecke GJ, Hochwald GM. The liver as the site of C-reactive protein formation. J Exp Med. 1966; 123(2):365-78. DOI: https://doi.org/10.1084/jem.123.2.365

Calabró P, Willerson JT. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation. 2003; 108(16):1930-2.

DOI: https://doi.org/10.1161/01.CIR.0000096055.62724.C5

Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation. 2000; 102(18):2165-8.

DOI: https://doi.org/10.1161/01.CIR.102.18.2165

Verma S, Kuliszewski MA, Li SH, Szmitko PE, Zucco L, Wang CH. C-reactive protein attenuates endothelial progenitor cell survival, differentiation, and function: further evidence of a mechanistic link between C-reactive protein and cardiovascular disease. Circulation. 2004; 109(17):2058-67.

DOI: https://doi.org/10.1161/01.CIR.102.18.2165

Wang CH, Li SH, Weisel RD, Fedak PW, Dumont AS, Szmitko P, et al. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle. Circulation. 2003; 107(13):1783-90.

DOI: https://doi.org/10.1161/01.CIR.0000061916.95736.E5

Hage FG, Oparil S, Xing D, Chen YF, McCrory MA, Szalai AJ. C-reactive protein-mediated vascular injury requires complement. Arteriosclerosis, Thrombosis, and Vascular Biology. 2010; 30(6):1189-95.

DOI: https://doi.org/10.1161/ATVBAHA.110.205377

Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation. 2005; 111(25):3481-8.

DOI: https://doi.org/10.1161/CIRCULATIONAHA.105.537878

Danesh J, Muir J, Wong YK, Ward M, Gallimore JR, Pepys MB. Risk factors for coronary heart disease and acute-phase proteins. A population-based study. Eur Heart J. 1999; 20(13):954-9. DOI: https://doi.org/10.1053/euhj.1998.1309

Tang WB, Zhou YQ, Zhao T, Shan JL, Sun P, Yang TT, et al. Effect of interleukin-6 (IL-6) on the vascular smooth muscle contraction in abdominal aorta of rats with streptozotocin-induced diabetes. Chin J Physiol. 2011; 54(5):318-23.

DOI: https://doi.org/10.4077/CJP.2011.AMM069

Steiner MK, Syrkina OL, Kolliputi N, Mark EJ, Hales CA, Waxman AB. Interleukin-6 overexpression induces pulmonary hypertension. Circ Res. 2009; 104(2):236-44.

DOI: https://doi.org/10.1161/CIRCRESAHA.108.182014

Iversen PO, Nicolaysen A, Kvernebo K, Benestad HB, Nicolaysen G. Human cytokines modulate arterial vascular tone via endothelial receptors. Pflügers Archiv. 1999; 439:93-100.

DOI: https://doi.org/10.1007/s004249900149

Empana JP, Jouven X, Canouï-Poitrine F, Luc G, Tafflet M, Haas B, et al . C-reactive protein, interleukin 6, fibrinogen and risk of sudden death in European middle-aged men: the PRIME study. Arterioscler Thromb Vasc Biol. 2010; 30(10):2047-52.

DOI: https://doi.org/10.1161/ATVBAHA.110.208785

Niida T, Isoda K, Kitagaki M, Ishigami N, Adachi T, Matsubara O, et al. IκBNS regulates interleukin-6 production and inhibits neointimal formation after vascular injury in mice. Card Res. 2012; 93(2):371-9.

DOI: https://doi.org/10.1093/cvr/cvr323

Rohde LE, Lee RT, Rivero J, Jamacochian M, Arroyo LH, Briggs W, et al. Circulating cell adhesion molecules are correlated with ultrasound-based assessment of carotid atherosclerosis. Arteriosclerosis, thrombosis, and vascular bioArterioscler Thromb Vasc Biollogy. 1998; 18(11):1765-70.

DOI: https://doi.org/10.1161/01.ATV.18.11.1765

Neves MF, Amiri F, Virdis A, Diep QN, Schiffrin EL. Role of aldosterone in angiotensin II-induced cardiac and aortic inflammation, fibrosis, and hypertrophy. Can J Physiol Pharmacol . 2005; 83(11):999-1006.

DOI: https://doi.org/10.1139/y05-068

Pueyo ME, Gonzalez W, Nicoletti A, Savoie F, Arnal JF, Michel JB. Angiotensin II stimulates endothelial vascular cell adhesion molecule-1 via nuclear factor-κB activation induced by intracellular oxidative stress. Arteriosclerosis, thrombosis, and vascular bioArterioscler Thromb Vasc Biollogy. 2000; 20(3):645-51.

DOI: https://doi.org/10.1161/01.ATV.20.3.645.

Published
2023-07-09
How to Cite
1.
Abbod L, Abd Algabar F. The cardiovascular system’s Renin-Angiotensin-Aldosterone System (RAAS). JSTMU [Internet]. 9Jul.2023 [cited 14May2024];6(1):45-0. Available from: https://j.stmu.edu.pk/ojs/index.php/jstmu/article/view/224
Section
Review Article (without Meta-analysis)