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Am J Physiol Heart Circ Physiol (June 24, 2004). doi:10.1152/ajpheart.00431.2004
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Submitted on May 6, 2004
Accepted on June 22, 2004

Opening of Ca2+-Activated K+ Channel Triggers Early and Delayed Preconditioning against Ischemia/Reperfusion Injury Independent of Nitric Oxide Synthases in Mice

Xiaoyin Wang1, Chang Yin1, Lei Xi1, and Rakesh C. Kukreja1*

1 Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, Va, USA

* To whom correspondence should be addressed. E-mail: rakesh{at}hsc.vcu.edu.

Opening of calcium-activated potassium channel (KCa) has been shown to confer early cardioprotection. It is unknown whether the opening of this channel also induces delayed cardioprotection. In addition, we determined the involvement of nitric oxide synthases, which have been implicated in cardioprotection induced by opening of mitochondrial KATP channels. Adult male ICR mice were pretreated with KCa opener, NS1619 either 10 min or 24 hrs prior to 30 min of global ischemia and 60 min of reperfusion (I/R) in Langendorff mode. Infusion of NS1619 (10 µM) for 10 min before I/R led to smaller infarct size as compared with the vehicle (DMSO)-treated group (P<0.05). This infarct-limiting effect of NS1619 was associated with improvement in ventricular functional recovery following I/R. The NS1619-induced protection was abolished by co-administration with KCa blocker - paxilline (1 µM). Similarly, pretreatment with NS1619 (1 mg/kg, i.p.) induced delayed protection 24 hrs later (P<0.05). Interestingly, the NS1619-induced late protection was not blocked by NOS inhibitor, L-NAME (15 mg/kg, i.p.). Unlike diazoxide (the opener of mitoKATP channels), NS1619 did not increase the expression of iNOS or eNOS. Western blot analysis demonstrated the existences of {alpha} and {beta} subunits of KCa in the mouse heart tissue. We conclude that opening of KCa leads to both early and delayed preconditioning effect through mechanism which is independent of nitric oxide.




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