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KATP channels do not mediate exercise‐induced preconditioning against post‐infarct apoptosis
Author(s) -
McGinnis Graham Ripley,
Miller Lindsey,
Irwin Jaquelin Megan,
Urbiztondo Zea,
Landrun Michael,
Nanayakkara Gayani,
Amin Rajesh,
Quindry John Carl
Publication year - 2011
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.25.1_supplement.1097.13
Subject(s) - tunel assay , apoptosis , ligation , ischemia , medicine , necrosis , pharmacology , chemistry , cardiology , biochemistry
Exercise preconditions against cardiac ischemia reperfusion (IR) injury by activation of the mitochondrial and sarcolemmal ATP sensitive K+ channels (mitoKATP & sarcKATP, respectively), though the extent of protection is unknown. Our purpose was to examine the role of these channels on exercise preconditioning against IR induced apoptosis & necrosis. Male Sprague Dawley rats were treadmill exercised for 3 d, 60 min/d, prior to surgically induced IR injury via coronary artery ligation (LAD)(50min I/120min R). Before surgery, pharmacological inhibitors for mitoKATP (5‐Hydroxydecanoate, 5HD) and sarcKATP (HMR‐1098) were administered at 10 mg/kg. Hearts were excised and assessed for apoptotic and necrotic biomarkers using TUNEL, TTC, and Western Blotting. The sarcKATP channel was essential to exercise preconditioning against necrosis (p=0.001) while niether the mitoKATP or sarcKATP were essential for antiapoptotic protection. Attenuation of apoptosis could not be explained by the bax:bcl‐2 ratio or the cleaved‐:total caspase 3 ratio.