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1-opioid
receptor agonist, reduces infarct size via activation of
Gi/o proteins and
KATP channels
1 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 2 Toray Industries, Basic Research Laboratories, Kanagawa 248, Japan
We have previously shown that delta (
)-opioid
receptors, most notably 1, are
involved in the cardioprotective effect of ischemic preconditioning
(PC) in rats; however, the mechanism by which -opioid
receptor-induced cardioprotection is mediated remains unknown.
Therefore, we hypothesized that several of the known mediators of
ischemic PC such as the ATP-sensitive potassium (KATP) channel and
Gi/o proteins are involved in the
cardioprotective effect produced by
1-opioid receptor activation.
To address these possibilities, anesthetized, open-chest Wistar rats
were randomly assigned to five groups. Control animals were subjected
to 30 min of coronary artery occlusion and 2 h of reperfusion. To
demonstrate that stimulating
1-opioid receptors produces
cardioprotection, TAN-67, a new selective
1-agonist, was infused for 15 min before the long occlusion and reperfusion periods. In addition, one
group received 7-benzylidenenaltrexone (BNTX), a selective
1-antagonist, before TAN-67. To
study the involvement of KATP
channels or Gi/o proteins in
1-opioid receptor-induced
cardioprotection, glibenclamide (Glib), a
KATP channel antagonist, or
pertussis toxin (PTX), an inhibitor of
Gi/o proteins, was administered
before TAN-67. Infarct size (IS) as a percentage of the area at risk
(IS/AAR) was determined by tetrazolium stain. TAN-67 significantly
reduced IS/AAR as compared with control (56 ± 2 to 27 ± 5%,
n = 5, P < 0.05). The cardioprotective effect of TAN-67 was completely abolished by BNTX, Glib, and PTX (51 ± 3, 53 ± 5, and 61 ± 4%,
n = 6 for each group, respectively). These results are the first to suggest that stimulating the
1-opioid receptor elicits a
cardioprotective effect that is mediated via Gi/o proteins and
KATP channels in the intact rat
heart.
glibenclamide; pertussis toxin; ischemic preconditioning
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