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Am J Physiol Heart Circ Physiol 278: H1211-H1217, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 4, H1211-H1217, April 2000

Nitric oxide-induced cardioprotection in cultured rat ventricular myocytes

Roby D. Rakhit1, Richard J. Edwards1, James W. Mockridge1, Anwar R. Baydoun1, Amanda W. Wyatt2, G. E. Mann2, and Michael S. Marber1

1 Department of Cardiology, St. Thomas' Hospital, and 2 Department of Physiology, Centre for Cardiovascular Biology and Medicine, Kings College, London SE1 7EH, United Kingdom

The aim of this study was to investigate the role of nitric oxide (NO) in a cellular model of early preconditioning (PC) in cultured neonatal rat ventricular myocytes. Cardiomyocytes "preconditioned" with 90 min of stimulated ischemia (SI) followed by 30 min reoxygenation in normal culture conditions were protected against subsequent 6 h of SI. PC was blocked by NG-monomethyl-L-arginine monoacetate but not by dexamethasone pretreatment. Inducible nitric oxide synthase (NOS) protein expression was not detected during PC ischemia. Pretreatment (90 min) with the NO donor S-nitroso-N-acetyl-L,L-penicillamine (SNAP) mimicked PC, resulting in significant protection. SNAP-triggered protection was completely abolished by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) but was unaffected by chelerythrine or the presence of glibenclamide and 5-hydroxydecanoate. With the use of RIA, SNAP treatment increased cGMP levels, which were blocked by ODQ. Hence, NO is implicated as a trigger in this model of early PC via activation of a constitutive NOS isoform. After exposure to SNAP, the mechanism of cardioprotection is cGMP dependent but independent of protein kinase C or ATP-sensitive K+ channels. This differs from the proposed mechanism of NO-induced cardioprotection in late PC.

guanosine 3'-cyclic monophosphate; nitric oxide synthase; ischemic preconditioning; protein kinase C; adenosine 5'-triphosphate-sensitive potassium channel


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