Early increase in K+ conductance during metabolic inhibition by cyanide in guinea pig ventricular myocytes.

Muramatsu, Hikaru; Satō, Ryōichi; Okumura, Hidemasa

doi:10.1272/jnms1923.57.308

Cited by 7 publications

(7 citation statements)

References 30 publications

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“…These data also support previous studies dealing with the mechanism of hypoxia-induced APD shortening, where substantial contribution of [Ca 2+ ] i -dependent elevation of I K1 to the early phase of shortening was demonstrated [31,36,37], in addition to the proposed changes in a few more [Ca 2+ ] i -modulated currents, like I CaL , I NCX , or I Cl . On the other hand, the present data, demonstrating an augmentation of I K1 in response to elevation of [Ca 2+ ] i , seem to contradict to findings of some other studies [10,13,28,29,46] reporting a reduced steady-state I K1 following a rise of [Ca 2+ ] i .…”

Section: +supporting

confidence: 91%

[Ca2+]i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium

Nagy

Acsai

Kormos

et al. 2013

Pflugers Arch - Eur J Physiol

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Section: +supporting

confidence: 91%

[Ca2+]i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium

Nagy

Acsai

Kormos

et al. 2013

Pflugers Arch - Eur J Physiol

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“…For example, Petrich et al (1991) [3] have shown that in the rabbit heart, hypoxia-induced early AP shortening and speeding up of the late phase of repolarization is sensitive to low concentrations of Ba 2+ , a specific blocker of I K1 . The early increase in I K1 , preceding the activation of K ATP channels, was also observed in guinea-pig cardiomyocytes during metabolic inhibition with cyanide (CN), a blocker of oxidative phosphorylation [4]. An increase in I K1 is also associated with atrial fibrillation [5], where the metabolic status of cardiac myocytes is probably also affected.…”

Section: Introductionmentioning

confidence: 93%

Cardiac IK1 underlies early action potential shortening during hypoxia in the mouse heart

Piao

McLerie

et al. 2007

Journal of Molecular and Cellular Cardiology

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It is established that prolonged hypoxia leads to activation of K ATP channels and action potential (AP) shortening, but the mechanisms behind the early phase of metabolic stress remain controversial. Under normal conditions I K1 channels are constitutively active while K ATP channels are closed. Therefore, early changes in I K1 may underlie early AP shortening. This hypothesis was tested using transgenic mice with suppressed I K1 (AAA-TG). In isolated AAA-TG hearts AP shortening was delayed by ∼24 s compared to WT hearts. In WT ventricular myocytes, blocking oxidative phosphorylation with 1 mM cyanide (CN; 28°C) led to a 29% decrease in APD90 within ∼3-5 min. The effect of CN was reversed by application of 100 μM Ba 2+ , a selective blocker of I K1 , but not by 10 μM glybenclamide, a selective blocker of K ATP channels. Accordingly, voltage-clamp experiments revealed that both CN and true hypoxia lead to early activation of I K1. In AAA-TG myocytes, neither CN nor glybenclamide or Ba 2+ had any effect on AP. Further experiments showed that buffering of intracellular Ca 2+ with 20 mM BAPTA prevented I K1 activation by CN, although CN still caused a 54% increase in I K1 in a Ca 2+-free bath solution. Importantly, both (i) 20 μM ruthenium red, a selective inhibitor of SR Ca 2+-release, and (ii) depleting SR by application of 10 μM ryanodine+1 mM caffeine, abolished the activation of I K1 by CN. The above data strongly argue that in the mouse heart I K1 , not K ATP , channels are responsible for the early AP shortening during hypoxia.

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“…Interestingly, suppression of I K1 in rabbit ventricular myocytes abolishes protection by ischemic preconditioning, a role commonly assigned to K ATP channels [149]. In contrast, several isolated reports indicate that I K1 may be upregulated during acute hypoxia/anoxia [150] or cyanide poisoning [151]. Recently, a strong evidence for this phenomenon was provided by Piao et al [152] who showed that in mice the early AP shortening during acute hypoxia is mediated by I K1 but not K ATP channels.…”

Section: General Pathophysiologymentioning

confidence: 99%

Cardiac strong inward rectifier potassium channels

Anumonwo¹,

Lopatin²

2010

Journal of Molecular and Cellular Cardiology

145

125

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Cardiac IK1 and IKACh are the major potassium currents displaying classical strong inward rectification, a unique property that is critical for their roles in cardiac excitability. In the last fifteen years, research on IK1 and IKACh has been propelled by the cloning of the underlying inwardly rectifying potassium (Kir) channels, the discovery of the molecular mechanism of strong rectification and the linking of a number of disorders of cardiac excitability to defects in genes encoding Kir channels. Disease-causing mutations in Kir genes have been shown experimentally to affect one or more of the following channel properties: structure, assembly, trafficking and regulation, with the ultimate effect of a gain-, or a loss-of-function of the channel. It is now established that IK1 and IKACh channels are heterotetramers of Kir2 and Kir3 subunits, respectively. Each homomeric Kir channel has distinct biophysical and regulatory properties, and individual Kir subunits often display different patterns of regional, cellular and membrane distribution. These differences are thought to underlie important variations in the physiological properties of IK1 and IKACh. It has become increasingly clear that the contribution of IK1 and IKACh channels to cardiac electrical activity goes beyond their long recognized role in the stabilization of resting membrane potential and shaping the late phase of action potential repolarization in individual myocytes, but extends to being critical elements determining the overall electrical stability of the heart.

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Early increase in K+ conductance during metabolic inhibition by cyanide in guinea pig ventricular myocytes.

Cited by 7 publications

References 30 publications

[Ca2+]i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium

[Ca2+]i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium

Cardiac IK1 underlies early action potential shortening during hypoxia in the mouse heart

Cardiac strong inward rectifier potassium channels

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