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α1‐adrenergic receptor activation mimics ischemic postconditioning
Author(s) -
Janota Danielle Marie,
Yun June
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1130.10
Subject(s) - myocyte , autophagy , propidium iodide , ischemia , stimulation , medicine , lactate dehydrogenase , reperfusion injury , receptor , programmed cell death , pharmacology , cardioprotection , cardiology , apoptosis , chemistry , biochemistry , enzyme
Ischemic postconditioning has been shown to reduce injury in response to ischemia/reperfusion. Because of limitations on the clinical use of ischemic postconditioning protocols, pharmacological agents that elicit a postconditioning (PostC) effect are highly desired. Previous studies have shown that stimulation of alpha1‐adrenergic receptors (α1‐ARs) is cardioprotective, thus, the objective of this study was to determine the effectiveness and investigate possible mechanisms of α1‐AR stimulation in PostC of cardiac myocytes. Adult rat ventricular myocytes and HL‐1 cardiac myocytes were subjected to simulated ischemia‐reperfusion injury. Cell membrane permeability, evaluated by measuring released lactate dehydrogenase (LDH) or propidium iodide uptake (PI), was used as an estimate of cell death. Lower amounts of LDH and PI uptake were detected when α1‐ARs were stimulated at the onset of reperfusion. Prior studies suggest that increased autophagy (ATG) following ischemia is protective. Addition of ATG activator rapamycin at reperfusion onset decreased cell death and was comparable to that observed with α1‐AR stimulation. Further, α1‐AR‐mediated reductions in cell death were reversed in the presence of ATG inhibitor, 3‐ Methyladenine. Our results suggest that α1‐AR stimulation at the onset of reperfusion can reduce cardiac myocyte death, which may be mediated through regulation of autophagy.