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Associations between Genetic Polymorphisms and Heart Rate Variability
Published in Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker, ECG Time Series Variability Analysis, 2017
Anne Voigt, Jasha W. Trompf, Mikhail Tamayo, Ethan Ng, Yuling Zhou, Yaxin Lu, Slade Matthews, Brett D. Hambly, Herbert F. Jelinek
Attention has largely been focused on genes encoding the angiotensin-converting enzyme (ACE). In diabetic neuropathy and HRV variability, it has been identified as a candidate gene in regard to its role in HRV. Differences in ACE concentration in plasma between individuals were linked to a major gene polymorphism (Rigat et al. 1990). ACE is a central player in the renin–angiotensin system (RAS) (Kennon et al. 1999), a cardiovascular regulatory system, which regulates cardiovascular function and BP (Nishikino et al. 2006). RAS has been shown to be elevated in patients with metabolic syndrome (MetS) (Sharma 2004), suggesting a link to CAN. ACE is involved in the activation of angiotensin II (Ang II), through which vascular contraction, renal function, fluid homeostasis, and sympathetic nerve activity are regulated. Ang II also leads to the production of reactive oxygen species (ROS), increasing oxidative stress and damaging NO synthases (Elton et al. 2010).
Lipase-Mediated Biocatalysis as a Greener and Sustainable Choice for Pharmaceutical Processes
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Monika Sharma, Tanya Bajaj, Rohit Sharma
Angiotensin-converting enzyme (ACE) is an important component of rennin-angiotensin system which exerts its effect on blood pressure by regulating the body fluids. ACE inhibitors are antihypertensive agents which function by inhibiting the activity of ACE, decreasing the production of angiotensin II and thus resulting in vasodilation. This activity reduces the overall blood pressure of the patient. Examples include classical “prils” like captopril, zofenopril, enalapril, ceranopril and lisinopril (Fig. 1.4). All of these drugs are given orally (P.O.) except for enalapril which can be administered intravenously. Also, all these ACE inhibitors are administered as prodrugs and require activation except for Lisinopril and captopril (Page, 2014).
Utilization of Fisheries' By-Products for Functional Foods
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Muhamad Darmawan, Nurrahmi Dewi Fajarningsih, Sihono, Hari Eko Irianto
FPHs have been reported as a superior source for various biological activities. One of the highlighted bioactivities of the fish protein hydrolysates is antihypertensive activity. ACE is able to catalyze the conversion of angiotensin I to the active angiotensin II (a vasoconstrictor) and inactivate bradykinin (a vasodilator), which results in the blood pressure increasing (Lee and Hur, 2017). The efficacy of ACE inhibitors in treating hypertension is well reported. It is also reported that natural ACE inhibitors are safer for long-term use than synthetic medicines (Kim and Wijesekara, 2010; Korczek et al., 2018). Thus, food-derived ACE inhibitors such as FPHs become important alternatives to these medicines (Zamora-Sillero et al., 2018).
Vitamin D supplementation alters the expression of genes associated with hypertension and did not induce DNA damage in rats
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Carla Da Silva Machado, Alexandre Ferro Aissa, Diego Luis Ribeiro, Lusânia Maria Greggi Antunes
The vitamin D3 deficient diet upregulated expression of nine genes in SHR rats (Ace, Agtr1b, Cacna1c, Drd5, Mylk2, Nostrin, Scnn1a, Scnn1g, and Sphk1) and six genes in normotensive WKY controls (Ace, Cacna1c, Ednra, Ephx2, Itpr1 and Itpr2). Ace was upregulated by vitamin D3 deficient diet in both SHR and normotensive WKY animals. The role of ACE in regulation of cardiovascular function and electrolyte homeostasis is well established, and ACE inhibitory molecules are commonly used in antihypertensive therapies (Cushman and Ondetti 1980; Danilczyk and Penninger 2006). Excess angiotensin II, ACE’s main active peptide, plays a critical role in cardiac ischemia occurrence, and our findings demonstrated that vitamin D3 deficiency increased Ace expression in both experimental models.
Atmospheric environment and severe acute respiratory infections in Nanjing, China, 2018–2019
Published in International Journal of Environmental Health Research, 2023
Kang-Jun Wu, Xiao-Qing Wu, Lei Hong
In this study, although the effect of NO2 on SARI was not statistically significant, the curves still showed that the hazard range was also concentrated in the high concentrations. Nitrogen oxide (NOx), particularly NO2, is derived from large emissions of vehicle exhaust, besides ambient temperature and humidity are essential regulators of NOx emissions (Grange et al. 2019). NO2 may cause pro-inflammatory and oxidative stress responses in the lungs, and long-term exposure to high NO2 can lead to impairment of lung function (Carbone et al. 2014; Mirowsky et al. 2016). Angiotensin-converting enzyme 2 (ACE2) is the leading agent of severe acute respiratory syndrome coronavirus (SARS-CoV) and severe respiratory syndrome coronavirus-2 (SARS-CoV-2) cellular receptors, which are highly expressed in alveolar epithelial cells, while NO2 can upregulate the expression level of ACE2 and increase the risk of viral infection (Alifano et al. 2020; Hoffmann et al. 2020). Likewise, High O3 caused an increased risk of SARI. Previous studies showed that increased concentrations of O3 might cause acute pulmonary function abnormalities in adolescents in small islands which was free of potential foreign contaminants (Yoda et al. 2017). O3 leads to the peroxidation of cell membrane surface lipids in respiratory mucosa and epithelial cells, causing cellular damage and inflammatory responses in the respiratory tract (Mumby et al. 2019). In addition, acute exposure to high O3 causes less rapid respiratory inflammation than lung injury with later metabolic abnormalities (Bromberg 2016; Shore 2019). The effect of CO was similar to those of the previously described air pollution. The acute effects of CO on humans was leading to shock and asphyxiation, due to the high affinity of CO binding to hemoglobin. Environmental concentration changes in CO are synchronized with carbon black as one of the components of PM2.5, and there may be synergistic effects of CO with carbon black (Liu et al. 2019).
The association of the ACTN3 R577X and ACE I/D polymorphisms with athlete status in football: a systematic review and meta-analysis
Published in Journal of Sports Sciences, 2021
Alexander B. T. McAuley, David C. Hughes, Loukia G. Tsaprouni, Ian Varley, Bruce Suraci, Thomas R. Roos, Adam J. Herbert, Adam L. Kelly
Another commonly investigated gene in sport performance is the angiotensin I converting enzyme (ACE) gene. The angiotensin I converting enzyme catalyses the degradation of the inactive decapeptide angiotensin I, and subsequently generates the physiologically active peptide, angiotensin II; an oligopeptide of eight amino acids that binds to specific receptors in the body affecting several systems (Dzau, 1988; Munzenmaier & Greene, 1996). Angiotensin II can constrict blood vessels and stimulate aldosterone production, resulting in increased blood pressure, thirst, or the dire for salt. As such, the ACE enzyme is the most crucial component of the renin-angiotensin system (RAS), as it is a potent vasopressor and aldosterone-stimulating peptide which regulates blood pressure and fluid–electrolyte balance (Erdös & Skidgel, 1987). A polymorphism has been identified within intron 16 of the ACE gene, located on chromosome 17q23.3 (NC_000017.11), which results in a substantial variation of RAS activity (Danser et al., 1995; Rigat et al., 1990). The polymorphism is known as an insertion/deletion (indel) polymorphism, with the insertion (I allele) and deletion (D allele) representing the presence and absence of a 287-bp Alu-sequence, respectively. Specifically, the I allele has been associated with lower serum and tissue ACE activity, alongside an increased percentage of slow-twitch (type I) muscle fibres; whilst the D allele has been associated with higher circulating and tissue ACE activity, alongside greater strength and muscle volume and an increased percentage of type II muscle fibres (Danser et al., 1995; Rigat et al., 1990; Zhang et al., 2003). In the context of sport, the I allele has been frequently associated with elite endurance performance. Specifically, higher I allele frequencies have been reported in middle- and long-distance rowers, swimmers, road-cyclists, runners, mountaineers, cross-country skiers, and tri-athletes across a range of diverse cohorts (e.g. British, Australian, Croatian, Russian, Spanish, Italian, Turkish, Polish, Japanese, Indian) (Alvarez et al., 2000; Cieszczyk et al., 2009; Gayagay et al., 1998; Min et al., 2009; Montgomery et al., 1998; Myerson et al., 1999; Nazarov et al., 2001; Scanavini et al., 2002; Shenoy et al., 2010; Turgut et al., 2004). Indeed, during the meta-analysis of Ma and colleagues (Ma et al., 2013), the authors also assessed the influence of the ACE I/D polymorphism on endurance athletes over 25 studies, reporting that the II genotype was significantly associated with endurance athletes. However, the authors found no association between the ACE I/D polymorphism and power athletes. This may have been due to the large heterogeneity observed between studies (I2 = >75%), most likely a result of not analysing the power athletes independently based upon ethnicity. Indeed, a more recent meta-analysis did conduct an ethnic-specific analysis of power athletes and reported significant associations with the ACE D allele (Weyerstraß et al., 2018).