Faculty Collaboration Database

Sarcolemmal K(ATP) channel triggers opioid-induced delayed cardioprotection in the rat. Circ Res 2002 Aug 09;91(3):186-8

Date

08/10/2002

Pubmed ID

12169643

DOI

10.1161/01.res.0000029085.69891.f2

Scopus ID

2-s2.0-0037047693 (requires institutional sign-in at Scopus site)   46 Citations

Abstract

Recently, the involvement of sarcolemmal K(ATP) (sarcK(ATP)) channels in ischemic and pharmacological preconditioning (IPC and PPC) has been minimized by numerous studies suggesting a primary role for mitochondrial K(ATP) (mitoK(ATP)) channels in early and delayed cardioprotection. Although the mitoK(ATP) channel has clearly been shown to be a distal effector of delayed IPC and PPC, studies implicating it as a trigger of protection in delayed IPC are lacking. Accordingly, we characterized the role of cardiac K(ATP) channels as triggers or distal effectors of delayed cardioprotection induced by opioids in rats, and the data suggest that the sarcK(ATP) channel triggers and that the mitoK(ATP) channel is a distal effector of opioid-induced delayed cardioprotection.

Author List

Patel HH, Hsu AK, Peart JN, Gross GJ

MESH terms used to index this publication - Major topics in bold

Adenosine Triphosphate
Animals
Benzamides
Cardiotonic Agents
Ischemic Preconditioning, Myocardial
Kinetics
Male
Myocardial Infarction
Piperazines
Potassium Channel Blockers
Potassium Channels
Rats
Rats, Sprague-Dawley
Receptors, Opioid, delta
Sarcolemma