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Cardiovascular PET-CT
Published in Yi-Hwa Liu, Albert J. Sinusas, Hybrid Imaging in Cardiovascular Medicine, 2017
Etienne Croteau, Ran Klein, Jennifer M. Renaud, Manuja Premaratne, Robert A. Dekemp
Beyond MBF and metabolism, the sympathetic nervous system, a component of the autonomic nervous system, can also be studied using PET-CT. Heart adrenergic receptor imaging of the sympathetic nerves has been used in diabetic, ischemic, and cardiac transplant states. Receptor density and function assessment may help improve the diagnosis and management of patients with heart failure following MI. Using the false neurotransmitter 11C-hydroxyephedrine (11C-HED), PET-CT dynamic imaging has shown that reduced retention (regional denervation) may be an early marker of CAD without evidence of MI (Thackeray and Bengel 2013) and i s associated with poor prognosis in patients receiving implantable cardioverter defibrillator (ICD) for primary prevention of ventricular fibrillation. As a second example, the renin-angiotensin system (RAS) is implicated in heart failure progression and cardiac remodeling following MI. Interest is increasing to develop strategies to mitigate the maladaptive mechanisms following myocardial injury. Medical therapies targeted at the RAS have demonstrated an outcome benefit after MI, whereas overexpression of angiotensin II type I (AT1R) has been associated with hypertrophy and fibrosis observed in the heart. 11C-KR31173 imaging of AT1R receptor density has been shown to predict the risk of adverse cardiac ventricular remodeling (Zober et al. 2006).
Arsenic, cadmium, and mercury-induced hypertension: mechanisms and epidemiological findings
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Airton da Cunha Martins, Maria Fernanda Hornos Carneiro, Denise Grotto, Joseph A Adeyemi, Fernando Barbosa
The renin–angiotensin system (RAS) plays a major role in blood pressure regulation. Under physiology and pathophysiology conditions, renin stimulation in kidneys leads to conversion of angiotensinogen into angiotensin I which is further converted into angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that raises blood pressure by increasing water retention, Na+ reabsorption, and secretion of K+ (Atlas 2007; Patel et al. 2017). Moreover, angiotensin II promotes vasoconstriction by inducing COX-2 protein expression, production of prostanoids, and NADPH oxidase activity (Angeli et al. 2013; Dos Santos et al. 2016; Rajagopalan et al. 1996).
COVID-19;-The origin, genetics,and management of the infection of mothers and babies
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hassan Ih El-Sayyad, Yousef Ka Abdalhafid
Changes to the renin-angiotensin system (RAS) are one of several causes of elevated blood pressure and atherosclerosis [40]. The activation of the RAS through angiotensin (II) development has weakened the cardiovascular system including hypertrophy of the left ventricule, increased perforation of the vascular wall smooth muscle and impaired vascular endothelial function [41]. The ACE2 In the RAS system, is a zinc-dependent metalloprotease, which catalyzes the conversion of angiotensin II to angiotensin I [42]. Notably the amount of ACE2 plasma differs between among patients [43].
The interplay between DNA methylation and cardiac autonomic system functioning: a systematic review
Published in International Journal of Environmental Health Research, 2023
Nayara Cristina Dos Santos Oliveira, Fernanda Serpeloni, Simone Gonçalves de Assis
Overall, thirty-three candidate loci were evaluated in different functions: Stress response cascade: Genes involved in the regulation of the hypothalamic-pituitary-adrenal (HPA)-axis, such as three glucocorticoid pathway genes – NR3C1 (the nuclear receptor subfamily 3 group C member 1) (de Rooij et al. 2012; Li-Tempel et al. 2016; Monk et al. 2016; Aghagoli et al. 2020), the co-chaperone of the glucocorticoid receptor – FKBP5 (FK506-binding protein 5), an enzyme that inactivates glucocorticoids – HSD11B2 (hydroxysteroid 11-beta dehydrogenase subtype 2) (Monk et al. 2016), as well as OXTR (oxytocin receptor) (Lancaster et al. 2018).Genes involved in the renin−angiotensin system: ACE (angiotensin-converting enzyme) (Wang et al. 2016; Xia et al. 2018), Ace2 (angiotensin I converting enzyme 2) (Mukerjee et al. 2017), Ace1 (angiotensin I converting enzyme 1) (Chu et al. 2015), EDN1 (endothelin-1) (Tobaldini et al. 2018; Xia et al. 2018), and Agt (angiotensinogen) (Chu et al. 2015).Inflammatory pathway genes: IFNγ (interferon γ), SATalpha (Spermidine/Spermine N1-Acetyltransferase Alpha), eNOS and iNOS (endothelial and inducible nitric oxide synthase), ICAM (intercellular adhesion molecule 1), TLR2 (toll-like receptor 2), TLR4 (toll-like receptor 4), and IL-6 (interleukin 6) (Tobaldini et al. 2018).Hypoxia signaling pathway-related: EPAS1 (endothelial PAS domain protein 1), EPO (erythropoietin), PPARa (peroxisome proliferator-activated receptor alpha), RXRa (retinoid X receptor-alpha) and long interspersed nuclear element-1 (LINE-1) (Childebayeva et al. 2019).Others: ANRIL (Antisense non-coding RNA in the INK4 locus) related to coronary heart disease (Murray et al. 2016). Plagl1 (pleomorphic adenoma gene-like 1) and H19 (H19 Imprinted Maternally Expressed Transcript) are placental imprinting genes (Xu et al. 2017). Transposable elements Alu and LINE-1 were related to air pollutant exposure (Fan et al. 2014; Wang et al. 2016; Tobaldini et al. 2018).