The protective effect of prior ischemia reperfusion adenosine A1 or A3 receptor activation in the normal and hypertrophied heart

Abstract

CCPA in both modes of treatment and Cl-IB-MECA, especially in the injected mode, were beneficial in protecting the normal and hypertrophied perfused isolated rat heart subjected to normothermic cardioplegic ischemia. This protection was partially related to the increased phosphorylation of p38 MAPK.

Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning

“…Ischemic or pharmacologic (e.g., adenosine-receptor agonist, propofol) preconditioning reduced infarct size in normotensive and hypertensive, hypertrophied rat hearts in vitro (Ebrahim et al, 2007;Hochhauser et al, 2007;King et al, 2012) and in vivo (Dai et al, 2009). Similarly, pharmacologic preconditioning with isoflurane 6 weeks after permanent coronary artery ligation reduced infarct size after ischemia/reperfusion in the remaining myocardium, although hearts exhibited a substantial compensatory hypertrophy.…”

Extracellular adenosine triphosphate and adenosine in cancer

“…Adenosine receptor signaling A1 and A3 adenosine receptors inhibit adenylyl cyclase and protein kinase A activity, thus decreasing intracellular cAMP levels, with studies revealing an important function in cardioprotection (Liang and Jacobson, 1998;Reichelt et al, 2005;Hochhauser et al, 2007), angiogenesis (Clark et al, 2007) and protection against septic shock (Gallos et al, 2005). A1 and A3 adenosine receptors have also been linked to phosphatidylinositol 3-kinase, mitogen-activated protein kinase and protein kinase C pathways (Hasko and Cronstein, 2004;Gessi et al, 2008).…”

The A3Adenosine Receptor: History and Perspectives

“…A 3 AR activation protects cardiomyocytes from hypoxia via phosphorylation of p38 MAPK, located downstream of the mitochondrial K ATP channel opening (Leshem-Lev et al, 2010). Accordingly, increased phosphorylation of p38 has been found after Cl-IB-MECA treatment, which proves beneficial, protecting the rat heart subjected to ischemia (Hochhauser et al, 2007). In contrast, activation of A 2A and A 3 ARs inhibits p38 MAPK and nuclear factor-kB (NF-kB) pathways in human synoviocytes (Varani et al, 2010c).…”