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Hypertension and Correlation to Cerebrovascular Change: A Brief Overview
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
Heba Kandil, Dawn Sosnin, Ali Mahmoud, Ahmed Shalaby, Ahmed Soliman, Adel Elmaghraby, Jasjit S. Suri, Guruprasad Giridharan, Ayman El-Baz
Cerebrovascular health and physiological changes, such as vascular remodeling, can provide important information about the risk for developing diseases like hypertension and dementia. It is estimated that roughly one-third of dementia cases could be prevented by treating the underlying cause [59], [60], which is often hypertension. Chronic systemic hypertension can cause temporary or permanent disability, especially when left untreated. Hypertension causes damage especially to smaller blood vessels, and significantly increases the risk for end-organ damage, with greatest concern focused mainly on the heart (e.g., heart failure, LVH), kidneys (e.g., renal failure), eyes (visual impairment), brain (e.g., dementia, stroke), and the lungs (pulmonary hypertension). It also contributes to early mortality. The Centers for Disease Control and Prevention (CDC) reports that in 2014, hypertension directly or indirectly affected the cause of death for over 400,000 people in the U.S. [61].
Cytochromes P450, Cardiovascular Homeostasis and Disease
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Chin Eng Ong, Amelia Dong, Boon Hooi Tan, Yan Pan
There is substantial evidence for the role of enzymes in the EET and HETE pathways, including CYPs and sEHs, in fluid and electrolyte homeostasis and blood pressure control. The best evidence was the report that male animals lacking sEH demonstrated high level of EETs, reduced renal production of DHETs (EET metabolites) and a significantly lower blood pressure (Sinal et al., 2000). In humans, blood EET level is reduced in women with pregnancy-induced hypertension (Catella et al., 1990) and in subjects with renovascular hypertension (Minuz et al., 2008). Moreover, significant drop in blood pressure was noted in different hypertensive models in rodents after the administration of a sEH inhibitor (Manhiani et al., 2009; Sinal et al., 2000). Substantial evidence in animals has also demonstrated that transgenic or overexpression of CYP epoxygenase lowered blood pressure in a number of hypertensive models. For example, recombinant adenovirus vector-mediated overexpression of CYP2J2 blocked blood pressure increase in spontaneously hypertensive rats (Xiao et al., 2010). In addition, the in vivo delivery of the homologous gene of CYP2J2 expressed mainly in rats, CYP2J3, enhanced EET level and reduced blood pressure in fructose-treated rats (Xu et al., 2010). EETs can potentially affect blood pressure through various mechanisms. These include modulation of the expression and activity of ion channels directly involved in the vasculature function and regulation of renal sodium excretion such as inwardly rectifying K channels, BK channels, or epithelial sodium channels (ENaCs) (Wang et al., 2008). BK channels, when activated, have been reported to cause hyperpolarization and relaxation of vascular smooth muscle cells (Ye et al., 2002). In addition to modulating the basal blood pressure, EETs can act via the modulation of the renin-angiotensin system. For example, sEH inhibitors showed their efficacy in hypertension associated with activation of the renin-angiotensin system (Imig, 2012). This is related to angiotensin II being a potent vasoconstrictor and a powerful inducer of sEH expression in the rat vasculature (Ai et al., 2007) as well as the rat heart (Ai et al., 2009). Recently, direct administration of EET analogs has been shown to demonstrate cardiovascular therapeutic potential when administered in vivo. One such compound is an 11,12-EET analog that was shown to lower blood pressure in spontaneously hypertensive rats (Sudhahar et al., 2010). Another compound is disodium (S)-2-(13-(3-pentyl)ureido)-tridec-8(Z)-enamido) succinate (EET-A), which demonstrated a direct vasodilatory effect and attenuated the development of hypertension in angiotensin II-infused rats (Červenka et al., 2018; Sporkova et al., 2017). Furthermore, EET-A has proven its effectiveness in experimental angiotensin II-dependent malignant hypertension, and attenuation of end-organ damage as a result of elevated pressure (Jichova et al., 2016).
Synthesis of Harvard Environmental Protection Agency (EPA) Center studies on traffic-related particulate pollution and cardiovascular outcomes in the Greater Boston Area
Published in Journal of the Air & Waste Management Association, 2019
Iny Jhun, Jina Kim, Bennet Cho, Diane R. Gold, Joel Schwartz, Brent A. Coull, Antonella Zanobetti, Mary B. Rice, Murray A. Mittleman, Eric Garshick, Pantel Vokonas, Marie-Abele Bind, Elissa H. Wilker, Francesca Dominici, Helen Suh, Petros Koutrakis
Long-term exposure to particulate air pollution increases risk of cardiovascular mortality in the general population (Di et al. 2017; Dockery et al. 1993; Miller et al. 2007; Pope et al. 2002). Residential proximity to a major roadway has been utilized as a surrogate for long-term traffic exposure to demonstrate associations with all-cause mortality (Finkelstein, Jerrett, and Sears 2004; Hoek et al. 2002), cardiopulmonary mortality (Gehring et al. 2006; Hoek et al. 2002), stroke mortality (Maheswaran and Elliott 2003), sudden cardiac death (Hart et al. 2014), and fatal coronary heart disease (Hart et al. 2014). In addition, living near a major road has been associated with myocardial infarction (Hart et al. 2013), hypertension (Kingsley et al. 2015), impaired conduit artery and microvascular function (Wilker et al. 2014), vascular end-organ damage (Van Hee et al. 2009), atherosclerosis (Hoffmann et al. 2007), and elevated C-reactive protein (CRP) levels (Lanki et al. 2015).