Role of endogenous nitric oxide in classic preconditioning in rat hearts

Prendes, María Gabriela Marina; González, Marcela; Savino, E.; Varela, A

doi:10.1016/j.regpep.2006.10.015

Cited by 17 publications

(6 citation statements)

References 39 publications

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“…It is probable that the attenuated cardioprotective effect of IPC in diabetic rat may be due to decreased availability of NO. Thus, NO appears to be responsible for cardioprotective effect of ischemic preconditioning [13]. However, in our study, treatment with sodium nitrite did not enhance the cardioprotective effect of IPC in normal rat.…”

Section: Discussioncontrasting

confidence: 68%

“…Brief episodes of ischemia followed by reperfusion of myocardium, increase the resistance against sustained ischemia of longer duration; this phenomenon is termed as ischemic preconditioning (IPC) [9]. IPC produces cardioprotection by PI-3K/Akt [10,11], phosphorylation of eNOS and by generation of nitric oxide (NO) and by opening of mito K ATP channel [12,13]. However, the cardioprotective effect of IPC is attenuated in conditions such as heart failure [14,15] aging [16,17] hypertension ([18,19] obesity [20] hyperlipidemia [21-23]and diabetes mellitus [24-26].…”

Section: Introductionmentioning

confidence: 99%

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Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart

Ajmani

Yadav

Singh

et al. 2011

BMC Cardiovasc Disord

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BackgroundNitric oxide (NO) has been noted to produce ischemic preconditioning (IPC)-mediated cardioprotection. Caveolin is a negative regulator of NO, which inhibits endothelial nitric oxide synthase (eNOS) by making caveolin-eNOS complex. The expression of caveolin is increased during diabetes mellitus (DM). The present study was designed to investigate the involvement of caveolin in attenuation of the cardioprotective effect of IPC during DM in rat.MethodsExperimental DM was induced by single dose of streptozotocin (50 mg/Kg, i.p,) and animals were used for experiments four weeks later. Isolated heart was mounted on Langendorff's apparatus, and was subjected to 30 min of global ischemia and 120 min of reperfusion. IPC was given by four cycles of 5 min of ischemia and 5 min of reperfusion with Kreb's-Henseleit solution (K-H). Extent of injury was measured in terms of infarct size by triphenyltetrazolium chloride (TTC) staining, and release of lactate dehydrogenase (LDH) and creatin kinase-MB (CK-MB) in coronary effluent. The cardiac release of NO was noted by measuring the level of nitrite in coronary effluent.ResultsIPC- induced cardioprotection and release of NO was significantly decreased in diabetic rat heart. Pre-treatment of diabetic rat with daidzein (DDZ) a caveolin inhibitor (0.2 mg/Kg/s.c), for one week, significantly increased the release of NO and restored the attenuated cardioprotective effect of IPC. Also perfusion of sodium nitrite (10 μM/L), a precursor of NO, significantly restored the lost effect of IPC, similar to daidzein in diabetic rat. Administration of 5-hydroxy deaconate (5-HD), a mito KATP channel blocker, significantly abolished the observed IPC-induced cardioprotection in normal rat or daidzein and sodium nitrite perfused diabetic rat heart alone or in combination.ConclusionsThus, it is suggested that attenuation of the cardioprotection in diabetic heart may be due to decrease the IPC mediated release of NO in the diabetic myocardium, which may be due to up -regulation of caveolin and subsequently decreased activity of eNOS.

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Section: Discussioncontrasting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart

Ajmani

Yadav

Singh

et al. 2011

BMC Cardiovasc Disord

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“…The ability of NOS inhibition or loss of NOS to block acute PC, however, has resulted in discrepant results. Some58, 59, but not all studies60, 61 find that NOS inhibitors block acute PC. Interestingly, although Downey's group initially reported that NOS inhibitors do not block acute PC60, Cohen, Downey and coworker54 recently reported the ability of L-NAME to block PC depends on the relative contribution of signaling through the adenosine pathways compared to the bradykinin or opioid pathways.…”

Section: No and Cardioprotectionmentioning

confidence: 99%

Protein S -Nitrosylation and Cardioprotection

Sun

Murphy

2010

Circulation Research

179

217

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“…Most recent studies have shown that IPC-induced cardioprotection is blocked by NOS inhibitors [6,13–16], and that mouse hearts lacking constitutive NOS are not protected by IPC [17,18], suggesting a role of NOS/NO signaling in acute IPC. In addition to activating sGC/cGMP/PKG signaling pathways, it has been shown that NO can directly modify protein sulfhydryl residues through protein S-nitros(yl)ation (SNO), which has emerged as an important posttranslational protein modification in cardiovascular signaling [19,20] and cardioprotection [21–23].…”

Section: Introductionmentioning

confidence: 99%

Essential role of nitric oxide in acute ischemic preconditioning: S-Nitros(yl)ation versus sGC/cGMP/PKG signaling?

Sun

Aponte

Kohr

et al. 2013

Free Radical Biology and Medicine

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Nitric oxide (NO) plays an important role in acute ischemic preconditioning (IPC). In addition to activating soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathways, NO-mediated protein S-nitros(yl)ation (SNO) has been recently shown to play an essential role in cardioprotection against ischemia–reperfusion (I/R) injury. In our previous studies, we have shown that IPC-induced cardioprotection could be blocked by treatment with either N-nitro-L-arginine methyl ester (L-NAME, a constitutive NO synthase inhibitor) or ascorbate (a reducing agent to decompose SNO). To clarify NO-mediated sGC/cGMP/PKG-dependent or -independent (i.e., SNO) signaling involved in IPC-induced cardioprotection, mouse hearts were Langendorff-perfused in the dark to prevent SNO decomposition by light exposure. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, a highly selective inhibitor of sGC) or KT5823 (a potent and selective inhibitor of PKG) did not abolish IPC-induced acute protection, suggesting that the sGC/cGMP/ PKG signaling pathway does not play an important role in NO-mediated cardioprotective signaling during acute IPC. In addition, treatment with ODQ in IPC hearts provided an additional protective effect on functional recovery, in parallel with a higher SNO level in these ODQ+IPC hearts. In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/ cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection.

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Role of endogenous nitric oxide in classic preconditioning in rat hearts

Cited by 17 publications

References 39 publications

Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart

Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart

Protein S -Nitrosylation and Cardioprotection

Essential role of nitric oxide in acute ischemic preconditioning: S-Nitros(yl)ation versus sGC/cGMP/PKG signaling?

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