ATP-dependent potassium channels involved in the cardiac protection induced by intermittent hypoxia against ischemia/reperfusion injury

Zhu, Haifeng; Dong, Jianwen; Zhu, Wuqiang; Ding, Huiping; Zhou, Zhao-Nian

doi:10.1016/s0024-3205(03)00429-6

Cited by 54 publications

(58 citation statements)

References 21 publications

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“…Adult and neonatal rats exhibited diminished frequency of ischemia-induced, K ATP channel-dependent arrhythmias, smaller infarct size and better postischemic contractility recovery following IH exposure (12,153,161). Furthermore, effects of IH adaptation were abolished by administration of K ATP channel blockers (glibenclamide, 5-hydroxydecanoate) while K ATP channel openers diazoxide (mitochondrial-selective) and pinacidil (general) mimicked the beneficial effects of IH in control animals (12,274 (129,142,163); and 3) regulation of mitochondrial volume and respiratory chain activity (126).…”

Section: Circulatory Systemmentioning

confidence: 99%

“…In addition to modulating Ca 2ϩ -handling pathways, the cardioprotective effects of IH have been independently attributed to mechanisms leading to opening of plasma and/or mitochondrial membrane K ATP channels (153,255,274,275). Adult and neonatal rats exhibited diminished frequency of ischemia-induced, K ATP channel-dependent arrhythmias, smaller infarct size and better postischemic contractility recovery following IH exposure (12,153,161).…”

Section: Circulatory Systemmentioning

confidence: 99%

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Hypoxia. 4. Hypoxia and ion channel function

Shimoda

Polàk

2011

American Journal of Physiology-Cell Physiology

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The ability to sense and respond to oxygen deprivation is required for survival; thus, understanding the mechanisms by which changes in oxygen are linked to cell viability and function is of great importance. Ion channels play a critical role in regulating cell function in a wide variety of biological processes, including neuronal transmission, control of ventilation, cardiac contractility, and control of vasomotor tone. Since the 1988 discovery of oxygen-sensitive potassium channels in chemoreceptors, the effect of hypoxia on an assortment of ion channels has been studied in an array of cell types. In this review, we describe the effects of both acute and sustained hypoxia (continuous and intermittent) on mammalian ion channels in several tissues, the mode of action, and their contribution to diverse cellular processes. oxygen deprivation; mammalian ion channels; oxygen homeostasis SENSING and appropriately responding to changes in O 2 concentration is of paramount importance for the survival of all organisms. Over time, O 2 homeostasis has evolved into a complex system to regulate O 2 delivery and use. While the rapid response to acute reductions in O 2 concentration typically results from processes that alter preexisting proteins, such as phosphorylation, stabilization, dimerization, or degradation, durable adaptation to prolonged hypoxic insult requires a coordinated response at the level of gene transcription. Since a deficit in O 2 is an important component of various physiological processes and the pathogenesis of numerous diseases, understanding the mechanisms by which changes in O 2 are linked to cell function is of great interest.Ion channels play a critical role in regulating a wide variety of biological processes, including neuronal transmission; control of ventillation; contraction of cardiac, skeletal, and smooth muscle; transport of nutrients and ions across the epithelium; T-cell activation; and glucose metabolism and pancreatic ␤-cell insulin release. To date, over 300 types of ion channels, differing in their mode of activation (voltage-dependent or -independent, ligand-gated, mechanosensitive, pH) and their ionic permeability (K ϩ , Ca 2ϩ , Cl Ϫ , Na ϩ ), have been identified. This heterogeneity in ion channel populations provides an astonishing array of variable responses within and between cell types. In 1988, a report demonstrating that rabbit carotid body glomus cells express an O 2 -sensitive potassium channel ushered in a new era of research exploring whether ion channel activity could be regulated in response to changes in O 2 availability (131). Since that initial description of an O 2 -regulated ion channel, an abundance of work has been produced indicating that a variety of ion channels spread across the different ion channel families are O 2 sensitive and exhibit changes in channel activity with acute hypoxia and alterations in channel quantity with prolonged hypoxic challenge. Although a great amount of work has been devoted to the study of hypoxia and ion channels in reptiles, amp...

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Section: Circulatory Systemmentioning

confidence: 99%

Section: Circulatory Systemmentioning

confidence: 99%

Hypoxia. 4. Hypoxia and ion channel function

Shimoda

Polàk

2011

American Journal of Physiology-Cell Physiology

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“…It is difficult to accurately simulate clinical myocardial I/R in a cellular model. We applied the model that was previously used to describe alterations in ventricular myocytes in the course of I/R (9), and many researchers used it (24,48).…”

Section: Discussionmentioning

confidence: 99%

“…Nawada et al (28) proposed that IPC protects the rabbit heart against the I/Rinduced reduction in Na/K pump activity, and inhibition of Na/K pump activity has been shown to attenuate the beneficial effect of IPC. CIHH has been shown to attenuate [Na ϩ ] i and Ca 2ϩ overloaded during I/R (8,48). Therefore, prevention of Ca 2ϩ overload by CIHH may involve changes in Na/K pump activity.…”

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confidence: 99%

Enhancement of Na/K pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury

Guo

Guo²,

Zhang³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Chronic intermittent hypobaric hypoxia (CIHH) has been shown to attenuate intracellular Na+ accumulation and Ca2+ overload during ischemia and reperfusion (I/R), both of which are closely related to the outcome of myocardial damage. Na/K pump plays an essential role in maintaining the equilibrium of intracellular Na+ and Ca2+ during I/R. It has been shown that enhancement of Na/K pump activity by ischemic preconditioning may be involved in the cardiac protection. Therefore, we tested whether Na/K pump was involved in the cardioprotection by CIHH. We found that Na/K pump current in cardiac myocytes of guinea pigs exposed to CIHH increased 1.45-fold. The K 1 and f 1, which reflect the portion of α1-isoform of Na/K pump, dramatically decreased or increased, respectively, in CIHH myocytes. Western blot analysis revealed that CIHH increased the protein expression of the α1-isoform by 76%, whereas the protein expression of the α2-isoform was not changed significantly. Na/K pump current was significantly suppressed in simulated I/R, and CIHH preserved the Na/K pump current. CIHH significantly improved the recovery of cell length and contraction during reperfusion. Furthermore, inhibition of Na/K pump by ouabain attenuated the protective effect afforded by CIHH. Collectively, these data suggest that the increase of Na/K pump activity following CIHH is due to the upregulating α1-isoform of Na/K pump, which may be one of the mechanisms of CIHH against I/R-induced injury.

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“…Until now, most studies on K ATP channel cardioprotection were carried out in experimental animals. However, the effect of THR on the heart is not well defined (Zhu et al, 2003). The objective of this study was to determine whether K ATP channels confer cardioprotection during reperfusion.…”

Section: Introductionmentioning

confidence: 99%

Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion

Dong

Zhu

2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to evaluate the cardioprotective effect of pinacidil postconditioning on rat hearts with transient hypoxia and reperfusion. An acute myocardial anoxia-reperfusion rat model was created by ligating coronary arteries for 10 min and subsequent reperfusion for 60 min. Twenty-four rats in 4 groups received different treatments: normal hearts as control (N = 6), anoxia-reperfusion (A/R) only (N = 6), pinacidil postconditioning (N = 6), and pinacidil plus adenosine triphosphate-sensitive potassium channel inhibitors (glibenclamide) (N = 6). The kinetic parameters and electrophysiological properties, including early apoptosis protein expression changes of Bax, Bcl-2, and FN were examined using the isolated perfusion and patch-clamp technique and immunohistochemistry. The left ventricular systolic pressure and maximum -dp/dt in A/R groups were significantly higher than those in the control group (P < 0.05). The left ventricular developing pressure, maximum +dp/dt, and heart rate in the A/R group were slightly decreased. The pinacidil-postconditioned group has better cardiac function recovery after ischemia/reperfusion than the A/R group (P < 0.01). In addition, using the patch-clamp technique, the mean open time and conductance values are significantly higher in the pinacidil postconditioning group, compared with those in the A/R group. The FN) increased during A/R, while Bcl-2 protein expression decreased. A significant difference was found in the pinacidil treatment group relative to the A/R group. Pinacidil postconditioning can exert cardioprotective effects on A/R-injured rat hearts, which may indicate a potential application of pinacidil postconditioning to protect A/R-injured hearts.

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ATP-dependent potassium channels involved in the cardiac protection induced by intermittent hypoxia against ischemia/reperfusion injury

Cited by 54 publications

References 21 publications

Hypoxia. 4. Hypoxia and ion channel function

Hypoxia. 4. Hypoxia and ion channel function

Enhancement of Na/K pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury

Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion

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