KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

Bu, Huimin; Yang, Cui; Wang, Meiling; Ma, Huijie; Sun, Hong; Zhang, Yi

doi:10.1007/s12576-015-0376-5

Cited by 24 publications

(18 citation statements)

References 22 publications

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“…In contrast, the selective sarcK ATP channel blocker HMR 1098 did not alter CCNH-induced tolerance to ischemia and reperfusion. This result is consistent with published data indicating the participation of mitoK ATP channel in the infarct-limiting effect of ischemic preconditioning (Yellon and Downey 2003) and adaptation to intermittent hypoxia (Kolar et al 2005;Bu et al 2015) Our studies and those of other investigators have documented that mitoK ATP channel is involved in the signaling pathway of cardioprotective effect of exogenous opioids (McPherson and Yao 2001;Peart et al 2008;Maslov et al 2009;Gross et al 2012). This result is consistent with published data on participation of opioid receptors in the infarct reducing effect of CCNH (Maslov et al 2013) and chronic intermittent hypoxia (Estrada et al 2016).…”

Section: Disscussionsupporting

confidence: 93%

“…The results of our experiments with atractyloside were somewhat unexpected since we had previously demonstrated that adaptation to chronic continuous hypoxia blocks the opening of MPT pore in response to ischemia/reperfusion of the isolated rat heart (Maslov et al 2015). It has been shown that atractyloside abolished infarct reducing effect chronic intermittent hypoxia (Bu et al 2015). Prior studies have shown that MPT pore plays an important role in the pathogenesis of apoptotic cell death (Halestrap 2010).…”

Section: Disscussionmentioning

confidence: 63%

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Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia

Tsibulnikov

Maslov²,

Naryzhnaya³

et al. 2018

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It was established that adaptation to chronic continuous normobaric hypoxia (CCNH) increases cardiac tolerance to ischemia and reperfusion. Coronary artery occlusion (20 min) and reperfusion (3 h) was performed in Wistar rats. CCNH promoted a decrease in the infarct size/ area at risk ratio in 2-fold. CCNH promoted an increase in the nitrite/nitrate levels in blood serum and myocardium. Pretreatment with protein kinase C (PKC) inhibitor chelerythrine, NO-synthase (NOS) inhibitor L-NAME, iNOS inhibitor S-methylisothiourea, K ATP channel blocker glibenclamide, mitoK ATP channel blocker 5-hydroxydecanoic acid abolished the infarct-reducing effect of CCNH. The non-selective tyrosine kinase inhibitor genistein attenuated but not eliminated infarct-sparing effect of CCNH. The nNOS inhibitor 7-nitroindazole, sarcK ATP channel blocker HMR 1098, MPT pore inhibitor atractyloside, PI3 kinase inhibitor wortmannin did not reverse infarct-limiting effect of CCNH. It was concluded that infarct-reducing effect of CCNH is mediated via PKC, iNOS activation and mitoK ATP channel opening. While nNOS, PI3 kinase, sarcK ATP channel, MPT pore are not involved in the development of CCNH-induced cardiac tolerance to impact of ischemia-reperfusion.

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Section: Disscussionsupporting

confidence: 93%

Section: Disscussionmentioning

confidence: 63%

Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia

Tsibulnikov

Maslov²,

Naryzhnaya³

et al. 2018

gpb

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“…Oxygen radicals produced during I/R are important factors for myocardial injury Bu et al 2015). In this study, the cardioprotective effects of Nari was canceled by non-specific K ATP blocker Gli and specific mitoK ATP blocker 5-HD, which suggests Nari protects heart against I/R injury through opening of K ATP , especially mitoK ATP .…”

Section: Discussionmentioning

confidence: 53%

“…Recently, one study showed that Nari exerts anti-ischemic effects on rat heart which is likely to be mediated by the activation of mitochondrial BK channels (Testai et al 2013). And another study reported that Nari attenuated pressure overload-induced cardiac hypertrophy (Zhang et al 2015). However，the mechanism of Nari protection on heart against I/R injury is far from clear.…”

Section: Introductionmentioning

confidence: 99%

The cardioprotective effect of naringenin against ischemia–reperfusion injury through activation of ATP-sensitive potassium channel in rat

Meng

Guo

et al. 2016

Can. J. Physiol. Pharmacol.

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Naringenin (Nari) has antioxidative and anti-atherosclerosis effects, and activation of ATP-sensitive potassium channel (KATP) can offer cardiac protection. We hypothesized that Nari protects the heart against ischemia–reperfusion (I–R) injury through activation of KATP. Isolated hearts from adult male Sprague-Dawley rats experienced a 30-min global ischemia followed by 60-min reperfusion (120 min for the infarct size determination). The hearts were treated with Nari (NARI); Nari plus glibenclamide (GLI), a non-specific ATP-sensitive potassium channel blocker (NARI+GLI); and Nari plus 5-hydroxy decanoic acid (5-HD), a mitochondrial membrane ATP-sensitive potassium channel blocker (NARI+5-HD). The left ventricular pressure, lactate dehydrogenates (LDH) in coronary effluent, superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardium, and myocardial infarct area were measured. Nari above 2.5 μmol/L improved the recovery of left ventricular function, decreased LDH in coronary effluent, and reduced myocardial infarct area. The SOD activity was increased and MDA was decreased in Nari-treated myocardium. The cardioprotective effect of Nari was canceled by GLI and 5-HD. In conclusion, Nari has a cardioprotective effect against I–R injury, which may be carried out through activating ATP-sensitive potassium channels in both cell and mitochondrial membrane, and enhancing myocardial antioxidant capacity.

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“…Chronic intermittent hypobaric hypoxia (CIHH), which is similar to ischemic preconditioning and high altitude hypoxia adaptation, confers cardiac protection against ischemia/reperfusion (I/R) injury in rats [6][7][8][9]. Enhancement of resistance against calcium overload is one of the striking mechanisms of CIHH.…”

Section: Introductionmentioning

confidence: 99%

PGC-1α Participates in the Protective Effect of Chronic Intermittent Hypobaric Hypoxia on Cardiomyocytes

Hua

Guo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Myocardial ischemia/reperfusion (I/R) or hypoxia/reoxygenation (H/R) injury is always characterized by Ca²⁺ overload, energy metabolism disorder and necrocytosis of cardiomyocytes. We showed previously that chronic intermittent hypobaric hypoxia (CIHH) improves cardiac function during I/R through improving cardiac glucose metabolism. However, the underlying cellular and molecular mechanisms of CIHH treatment improving energy metabolism in cardiomyocytes are still unclear. In this study, we determined whether and how CIHH protects cardiomyocytes from Ca²⁺ overload and necrocytosis through energy regulating pathway. Methods: Adult male Sprague-Dawley rats were randomly divided into two groups: control (CON) and CIHH group. CIHH rats received a hypobaric hypoxia simulating 5,000-m altitude for 28 days, 6 hours each day, in hypobaric chamber. Rat ventricular myocytes were obtained by enzymatic dissociation. The intracellular calcium concentration ([Ca²⁺]_i) and cTnI protein expression were used to evaluate the degree of cardiomyocytes injury during and after H/R. The mRNA and protein expressions involved in cardiac energy metabolism were determined using quantitative PCR and Western blot techniques. PGC-1α siRNA adenovirus transfection was used to knock down PGC-1α gene expression of cardiomyocytes to determine the effect of PGC-1α in the energy regulating pathway. Results: H/R increased [Ca²⁺]_i and cTnI protein expression in cardiomyocytes. CIHH treatment decreased [Ca²⁺]_i (p< 0.01) and cTnI protein expression (p< 0.01) in cardiomyocytes after H/R. Both mRNA and protein expression of PGC-1α increased after CIHH treatment, which was reversed by PGC-1α siRNA adenovirus transfection. Furthermore, CIHH treatment increased the expression of HIF-1α, AMPK and p-AMPK in cardiomyocytes, and pretreatment with AMPK inhibitor dorsomorphin abolished the enhancement of PGC-1α protein expression in cardiomyocytes by CIHH (p< 0.01). In addition, PGC-1α knock down also abolished the increased protein level of GLUT4 (p< 0.01) and decreased the protein level of CPT-1b (p< 0.05) in cardiomyocytes by CIHH treatment. Conclusion: CIHH treatment could reduce the calcium overload and H/R injury in cardiomyocytes by up-regulating the expression of PGC-1α and regulating the energy metabolism of glucose and lipid. The HIF-1α-AMPK signaling pathway might be involved in the process.

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KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

Cited by 24 publications

References 22 publications

Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia

Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia

The cardioprotective effect of naringenin against ischemia–reperfusion injury through activation of ATP-sensitive potassium channel in rat

PGC-1α Participates in the Protective Effect of Chronic Intermittent Hypobaric Hypoxia on Cardiomyocytes

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