Ethanol inhibition of Ca2+ and Na+ currents in the guinea-pig heart

Habuchi, Yoshizumi; Furukawa, Taiji; Tanaka, Hideo; Lu, Lingling; Morikawa, Junichiro; Yoshimura, Manabu

doi:10.1016/0926-6917(95)90006-3

Cited by 43 publications

(36 citation statements)

References 21 publications

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“…Even though, in principle, observational studies do not allow for proof of causality, there are several theoretically plausible speculations for the cause-effect relationship between high alcohol intake and the development of AF. One speculation is based on biological findings that suggest a harmful effect of high alcohol intake on maintenance of normal heart rhythm, including the achievement of a hyperadrenergic state (32), impairment of vagal tone (33), direct effect on myocardial structure (34), and various electrophysiological changes in atrial cells (e.g., increase in intra-atrial conduction time represented by a length of the P-wave, reduction in the refractory period, negative inotropic effect through calcium-channel inhibition in ventricular cells) (31,35,36).…”

Section: Discussionmentioning

confidence: 99%

Alcohol Consumption and Risk of Atrial Fibrillation

Kodama

Saito

Tanaka

et al. 2011

Journal of the American College of Cardiology

259

136

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Section: Discussionmentioning

confidence: 99%

Alcohol Consumption and Risk of Atrial Fibrillation

Kodama

Saito

Tanaka

et al. 2011

Journal of the American College of Cardiology

259

136

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“…An effect of ethanol on myofilament sensitivity has been described and may contribute to the negative inotropic effect observed at 0.3 % ethanol [6,20,21]. Electrophysiological experiments investigating the effects of ethanol on the Ltype Ca currents have shown a threshold of 0.15 % ethanol for current inhibition at 37 mC [22]. Analyses of the effects of ethanol on the timing of peak shortening in multicellular preparations have produced discrepant findings, probably due, at least partly, to the use of low stimulus frequencies [23,24].…”

Section: Mechanisms Of Action Of Ethanolmentioning

confidence: 99%

Ethanol effects on cardiomyocyte contractility

DELBRIDGE¹,

CONNELL²,

HARRIS³

et al. 2000

Clinical Science

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Little is known about the direct cardiac effects of socially common sub-intoxication levels of ethanol. Previous studies evaluating the responses of normal cardiomyocytes to short-term ethanol exposure have utilized ethanol concentrations equivalent to extreme intoxication or lethal levels in vivo. The purpose of the present study was to investigate the contractile responses of isolated rat ventricular cardiomyocytes during exposure to relatively low concentrations of ethanol in the range 0.05-0.5% (v/v) (8.6-86 mM) under physiological conditions (3 Hz stimulation; 36 degrees C; BSA vehicle). High-speed imaging techniques were used to study the kinetics of myocyte contraction, and shortening parameters were calculated for mechanistic evaluation. The concentration-response relationship was not linear and exhibited two plateau phases, suggesting at least two mechanisms of action of ethanol on cardiomyocyte contraction. At 0.05% (8.6 mM), ethanol treatment produced a 14.4% decrease in maximum myocyte shortening. The maximum rates of cell shortening and lengthening were similarly impaired, but there was no effect on contraction cycle timing at this low concentration. At 0.30% (51 mM), ethanol reduced maximum shortening by 40.2%, prolonged excitation-contraction coupling latency and abbreviated the contraction cycle time by 38%. The inotropic modulatory effect of ethanol was exaggerated in the absence of protein in the superfusion buffer. This is the first report which identifies ethanol at 0.05% (v/v) as a modulator of cardiac contractility. Kinetic analyses indicate that the mechanism of action involves disturbance of sarcoplasmic reticulum function, and this may contribute to arrhythmogenic vulnerability - especially in an in vivo context of heightened compensatory sympathetic drive.

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“…Earlier studies have shown that ethanol (80 mM) significantly inhibited sodium channel by 1375% on guinea pig ventricular cells [7]. In the dorsal root ganglion neurons, ethanol (200 mM) decreased both tetrodotoxin (TTX)-resistant and TTX-sensitive Na + currents [8].…”

Section: Introductionmentioning

confidence: 96%

Ethanol inhibits voltage-gated sodium channels in cultured superior cervical ganglion neurons

Xiao

Liu

et al. 2008

NeuroReport

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To determine whether actions on sodium channels contribute to ethanol's depressant effects on the autonomic nervous system, the acute effects of ethanol on Na+ currents in primary cultured superior cervical ganglion were examined by whole-cell patch clamp recordings. Ethanol inhibited Na+ currents concentration dependently, and decreased action potential firing. Ethanol (100 mM) did not affect activation curve, but resulted in a left shift of the inactivation curve and prolonged the recovery from inactivation. This finding indicates that the channels in the inactivated state are more susceptible to ethanol than those in the resting state. For the first time, this study demonstrates acute inhibitory effects of ethanol on sodium channel gating in sympathetic neurons.

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Ethanol inhibition of Ca2+ and Na+ currents in the guinea-pig heart

Cited by 43 publications

References 21 publications

Alcohol Consumption and Risk of Atrial Fibrillation

Alcohol Consumption and Risk of Atrial Fibrillation

Ethanol effects on cardiomyocyte contractility

Ethanol inhibits voltage-gated sodium channels in cultured superior cervical ganglion neurons

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