Biochemical and Biophysical Research Communications
Regular ArticleIdentification of Adenosine A2 Receptor-cAMP System in Human Aortic Endothelial Cells
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Crosstalk between adenosine receptors and CYP450-derived oxylipins in the modulation of cardiovascular, including coronary reactive hyperemic response
2022, Pharmacology and TherapeuticsCitation Excerpt :Adenosine is an endogenous nucleoside involved in various biological functions and is found in every tissue and organ (Jackson et al., 2002; Nayeem et al., 2003; Nayeem & Mustafa, 2002a, 2002b; Ralevic & Burnstock, 1998), and the adenosine is known to regulate blood flow in coronary arteries (Berne, 1963; Hanif et al., 2017) and exerts vasodilatory effects in almost all blood vessels of mammalians (Mubagwa, Mullane, & Flameng, 1996). The vasodilatory effects are due to the activation of adenosine A2A receptors (Belardinelli et al., 1998; Iwamoto et al., 1994; Nayeem et al., 2008; Nayeem et al., 2009; Nayeem et al., 2010; Nayeem et al., 2013; Nayeem, Zeldin, Boegehold, & Falck, 2011; Shryock et al., 1998) and adenosine A2B receptors (Yadav et al., 2015) through the production of cAMP in vascular smooth muscle cells (Iwamoto et al., 1994) and with the involvement of KATP channels and CYP450-epoxygenase pathways, in mouse aorta and coronary arteries (Agba, Hanif, Edin, Zeldin, & Nayeem, 2020; Hanif et al., 2017b; Hanif, Edin, Zeldin, & Nayeem, 2020; Nayeem et al., 2013; Ponnoth, Nayeem, Tilley, Ledent, & Jamal Mustafa, 2012; Pradhan, Ledent, Mustafa, Morisseau, & Nayeem, 2015). Therefore, A2AR KO (A2AAR−/−) mice showed signs of hypertension (Ledent et al., 1997), and also the adenosine shortens the action potential and increases refractoriness is due to the activation of A1AR (Belardinelli, Giles, & West, 1988; Mustafa, Morrison, Teng, & Pelleg, 2009; Pelleg, Hurt, & Hewlett, 1996).
Pharmacological profile of adenosine A <inf>2A</inf> receptors in patients with lower extremity peripheral artery disease and associated coronary artery disease: A pilot study
2019, International Journal of CardiologyCitation Excerpt :Adenosine triphosphate and adenosine contribute to the restoration of blood flow during ischemia [9], and play a major role in the control of the associated inflammation process [7]. Adenosine exerts its vasodilatory and anti-inflammatory effects mainly through activation of the A2A receptor (A2AR) [10] and the A2B receptor [11,12], which leads to an increase in production of cyclic adenosine monophosphate (cAMP) [10]. The production of cAMP has been correlated with vasodilatation [13].
Expressions of adenosine A<inf>2A</inf> receptors in coronary arteries and peripheral blood mononuclear cells are correlated in coronary artery disease patients
2017, International Journal of CardiologyCitation Excerpt :Here, we found that A2AR were also expressed in human aortic tissues. It was shown that aorta vasodilation implicates A2AR [23]. Thus, A2AR is involved in the control of blood pressure and high levels of A2AR expression on PBMC are associated with high blood pressure [24].
Ticagrelor increases adenosine plasma concentration in patients with an acute coronary syndrome
2014, Journal of the American College of CardiologyCitation Excerpt :Second, several lines of evidence confirmed the vasodilatory properties of adenosine on arterial beds (21). These properties could be related to the activation of low-affinity A2A receptors through the increase in APC, as these receptors are strongly implicated in coronary blood flow regulation (21,22). Accordingly, the APC level measured in the present study in the ticagrelor group is compatible with the activation of the adenosine A2A low affinity receptors (21).
Pharmacologic manipulation of coronary vascular physiology for the evaluation of coronary artery disease
2013, Pharmacology and TherapeuticsCitation Excerpt :Recent work has demonstrated that while the coronary vasodilatory effect can largely be ascribed to activation of adenosine A2A receptors (Belardinelli et al., 1998), activation of adenosine A2B receptors may also have a role (Morrison et al., 2002; Berwick et al., 2010). Although adenosine induces endothelium-mediated, NO-dependent vasodilation of epicardial coronary arteries (Vials & Burnstock, 1993; Iwamoto et al., 1994; Abebe et al., 1995) and the microvasculature (Lynch et al., 2006), much of the effect is likely mediated by arteriolar vasodilation, which involves both endothelial NO-dependent pathways and direct action on ATP-sensitive potassium channels in arteriolar smooth muscle (Hein et al., 1999; Berwick et al., 2010), although the degree of endothelial-dependence may be limited in humans with coronary atherosclerosis (Sato et al., 2005). This is supported by the finding that the degree of epicardial coronary arterial diameter increase is strongly related to the blood flow velocities (Lupi et al., 1997), suggesting that epicardial coronary artery dilation is through a flow-mediated endothelium-dependent mechanism (Rubanyi et al., 1986).